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Fiala, Pavel, Tomas Jirku, and I. Behunek. "Numerical Model of Inductive Flowmeter." PIERS Online 3, no. 5 (2007): 704–8. http://dx.doi.org/10.2529/piers061006093241.
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Drexler, P., P. Fiala, R. Kadlec, P. Londak, T. Madrova, M. Klima, and J. Zukal. "Numerical modeling and experimental verification of a low fluid flow inductive flowmeter." Flow Measurement and Instrumentation 78 (April 2021): 101876. http://dx.doi.org/10.1016/j.flowmeasinst.2020.101876.
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Bera, S. C., J. K. Ray, and S. Chattopadhyay. "A modified inductive pick-up type technique of measurement in a vortex flowmeter." Measurement 35, no. 1 (January 2004): 19–24. http://dx.doi.org/10.1016/j.measurement.2003.08.019.
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Osadchuk, A. V., V. S. Osadchuk, I. A. Osadchuk, D. R. Ilchuk, and G. A. Pastushenko. "Solid state radio-measuring optical-frequency transducer of gas flow rate." Physics and Chemistry of Solid State 22, no. 2 (April 20, 2021): 224–32. http://dx.doi.org/10.15330/pcss.22.2.224-232.
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The paper presents a study of a solid state radio-measuring optical-frequency transducer of gas consumption based on a transistor structure with a negative differential resistance. A mathematical model of a solid state radio-measuring optical-frequency flowmeter was developed, which made it possible to obtain the conversion function and the sensitivity equation. The solid state radio-measuring optical-frequency gas flowmeter is based on a transistor structure with a negative differential resistance, consisting of a HEMT field-effect transistor and a bipolar transistor with a passive inductive element. When replacing the passive inductance with an active inductive element, the transducer can be completely integrated. The negative differential resistance formed by the parallel connection of the impedance with the capacitive component on the collector-drain electrodes of the transistor structure and inductance leads to the occurrence of electrical oscillations in the oscillator circuit. Theoretical and experimental studies have shown that with an increase in gas consumption from 0 l/h to 4 l/h, the generation frequency decreases from 812.65 MHz to 811.62 MHz at a supply voltage of 3.3 V, and at a supply voltage of 3.8 V from 813.00 MHz to 811.80 MHz. It is shown that by choosing a constant voltage power supply mode, it is possible to obtain an almost linear dependence of the generation frequency on the gas flow rate and choose channels for transmitting measurement information. The obtained theoretical and experimental studies are in good agreement, the relative error does not exceed 2.5 %.
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Tozzi, Piergiorgio, Audrey Maertens, Jonathan Emery, Samuel Joseph, Matthias Kirsch, and François Avellan. "An Original Valveless Artificial Heart Providing Pulsatile Flow Tested in Mock Circulatory Loops." International Journal of Artificial Organs 40, no. 12 (November 8, 2017): 683–89. http://dx.doi.org/10.5301/ijao.5000634.
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Purpose We present the test bench results of a valveless total artificial heart that is potentially compatible with the pediatric population. Methods The RollingHeart is a valveless volumetric pump generating pulsatile flow. It consists of a single spherical cavity divided into 4 chambers by 2 rotating disks. The combined rotations of both disks produce changes in the volumes of the 4 cavities (suction and ejection). The blood enters/exits the spherical cavity through 4 openings that are symmetrical to the fixed rotation axis of the first disk. Mock circulatory system: The device pumps a 37% glycerin solution through 2 parallel circuits, simulating the pulmonary and systemic circulations. Flow rates are acquired with a magnetic inductive flowmeter, while pressure sensors collect pressure in the left and right outflow and inflow tracts. In vitro test protocol: The pump is run at speeds ranging from 20 to 180 ejections per minute. The waveform of the pressure generated at the inflow and outflow of the 4 chambers and the flow rate in the systemic circulation are measured. Results At an ejection rate of 178 min−1, the Rolling Heart pumps 5.3 L/min for a systemic maximal pressure gradient of 174 mmHg and a pulmonary maximal pressure gradient of 75 mmHg. The power input was 14 W, corresponding to an efficiency of 21%. Conclusions The Rolling Heart represents a new approach in the domain of total artificial heart. This preliminary study endorses the feasibility of a single valveless device acting as a total artificial heart.
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Умнова, А. В., А. С. Алейник, В. Е. Стригалев, В. А. Новикова, and А. Н. Аширов. "Датчик скорости потока жидкости на основе волоконных брэгговских решеток с индукционным нагревом." Письма в журнал технической физики 47, no. 17 (2021): 22. http://dx.doi.org/10.21883/pjtf.2021.17.51381.18816.
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The paper presents simulating and experimental results of flowmeter operation with induction heating, where fiber Bragg gratings were used as sensitive elements of temperature sensors. The operating principle of flowmeter based on cross-correlation method. During the experiment, it was detected time response of heat pulse from 0.2 s to 0.5 s that corresponds to a flow velocity range 0.1-0.5 m/s.
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Horner, Boris. "A novel profile-insensitive multi-electrode induction flowmeter suitable for industrial use." Measurement 24, no. 3 (October 1998): 131–37. http://dx.doi.org/10.1016/s0263-2241(98)00048-7.
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Horner, B., F. Mesch, and A. Trächtler. "A multi-sensor induction flowmeter reducing errors due to non-axisymmetric flow profiles." Measurement Science and Technology 7, no. 3 (March 1, 1996): 354–60. http://dx.doi.org/10.1088/0957-0233/7/3/016.
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Houben, Thijs, Inge CM Loonen, Serapio M. Baca, Maarten Schenke, Johanna H. Meijer, Michel D. Ferrari, Gisela M. Terwindt, et al. "Optogenetic induction of cortical spreading depression in anesthetized and freely behaving mice." Journal of Cerebral Blood Flow & Metabolism 37, no. 5 (July 20, 2016): 1641–55. http://dx.doi.org/10.1177/0271678x16645113.
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Cortical spreading depression, which plays an important role in multiple neurological disorders, has been studied primarily with experimental models that use highly invasive methods. We developed a relatively non-invasive optogenetic model to induce cortical spreading depression by transcranial stimulation of channelrhodopsin-2 ion channels expressed in cortical layer 5 neurons. Light-evoked cortical spreading depression in anesthetized and freely behaving mice was studied with intracortical DC-potentials, multi-unit activity and/or non-invasive laser Doppler flowmetry, and optical intrinsic signal imaging. In anesthetized mice, cortical spreading depression induction thresholds and propagation rates were similar for invasive (DC-potential) and non-invasive (laser Doppler flowmetry) recording paradigms. Cortical spreading depression-related vascular and parenchymal optical intrinsic signal changes were similar to those evoked with KCl. In freely behaving mice, DC-potential and multi-unit activity recordings combined with laser Doppler flowmetry revealed cortical spreading depression characteristics comparable to those under anesthesia, except for a shorter cortical spreading depression duration. Cortical spreading depression resulted in a short increase followed by prolonged reduction of spontaneous active behavior. Motor function, as assessed by wire grip tests, was transiently and unilaterally suppressed following a cortical spreading depression. Optogenetic cortical spreading depression induction has significant advantages over current models in that multiple cortical spreading depression events can be elicited in a non-invasive and cell type-selective fashion.
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Orlandi, C., C. J. Dunn, and L. G. Cutshaw. "Evaluation of angiogenesis in chronic inflammation by laser-Doppler flowmetry." Clinical Science 74, no. 2 (February 1, 1988): 119–21. http://dx.doi.org/10.1042/cs0740119.
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1. A non-invasive method is described for the assessment of angiogenesis in chronic inflammation using laser-Doppler flowmetry. 2. Significant increases in capillary blood flow were seen on days 5 and 7 after induction of subcutaneous granulomatous lesions, as compared with control skin. 3. Changes in blood flow were accompanied by changes in pulsatile flow pattern and by an intense angiogenic response observed by light microscopy. 4. The potential application of laser-Doppler flowmetry to quantitative and qualitative studies of evolving angiogenesis in pathological responses is discussed.
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Morelli, Andrea, Luigi Tritapepe, Monica Rocco, Giorgio Conti, Alessandra Orecchioni, Andrea De Gaetano, Umberto Picchini, Paolo Pelaia, Carlo Reale, and Paolo Pietropaoli. "Terlipressin versus Norepinephrine to Counteract Anesthesia-induced Hypotension in Patients Treated with Renin-Angiotensin System Inhibitors: Effects on Systemic and Regional Hemodynamics." Anesthesiology 102, no. 1 (January 1, 2005): 12–19. http://dx.doi.org/10.1097/00000542-200501000-00006.
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Background Terlipressin has been suggested as the ideal drug to treat anesthesia-induced hypotension in patients under long-term renin-angiotensin system inhibitor treatment for arterial hypertension. The authors compared the effects of terlipressin and norepinephrine on systemic hemodynamic parameters and gastric mucosal perfusion using a laser Doppler flowmetry technique in patients treated with renin-angiotensin system inhibitors who experienced hypotension at induction of anesthesia. Methods Thirty-two patients scheduled for carotid endarterectomy under general anesthesia and treated with renin-angiotensin system inhibitors had hypotension after induction of general anesthesia. They were randomized to receive 1 mg of terlipressin (n = 16) or norepinephrine infusion (n = 16) to counteract anesthesia-induced hypotension. A laser Doppler probe was introduced into the gastric lumen. All measurements were performed just before surgery, during hypotension, at 30 min, and at 4 h. Results Terlipressin produced an increase in mean arterial pressure and a decrease in gastric mucosal perfusion detected by laser Doppler flowmetry (P < 0.05) over 30 min that were sustained for 4 h. During the infusion, norepinephrine produced an increase in mean arterial pressure and in gastric mucosal perfusion detected by laser Doppler flowmetry (P < 0.05). If compared to norepinephrine, terlipressin reduced oxygen delivery and oxygen consumption (P < 0.05) and increased arterial lactate concentrations (P < 0.05). Conclusion This study showed the efficacy of terlipressin in the treatment of hypotension episodes in anesthetized patients chronically treated with renin-angiotensin system inhibitors, angiotensin converting-enzyme inhibitors, and angiotensin II receptor antagonists. However, the negative effects on gastric mucosal perfusion and the risk of iatrogenic oxygen supply dependency of terlipressin need to be taken into account.
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Ge, Liang, Yang He, Guiyun Tian, Guohui Wei, Junaid Ahmed, Hongxia Deng, and Qi Huang. "Measurement of Annular Flow for Drilling Engineering by Electromagnetic Flowmeter Based on Double-Frequency Excitation." Journal of Sensors 2019 (November 18, 2019): 1–14. http://dx.doi.org/10.1155/2019/4090632.
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Using downhole annular electromagnetic flow measurement to obtain annular flow in real-time is a foundation of microflow control drilling technology. The existing annular flow electromagnetic measurement method based on low-frequency rectangular excitation is affected by slurry interference and formation fluid invasion, which results in large noise generated on the electrode output signal. These noise causes the instability of the flow measurement system output and lower accuracy. Double-frequency rectangular wave excitation has the advantages of excellent zero-point stability attributed to low-frequency rectangular wave excitation and fast response speed with great ability to suppress slurry interference. First, the double-frequency rectangular wave excitation for annular flow electromagnetic measurement is researched, and its corresponding electromagnetic induction signal process is investigated. In order to verify the feasibility of downhole annular electromagnetic flow measurement, a flow verification platform for comparison of standard and detected parameters is established for simulation experiment, and the ability to suppress slurry interference and response speed of the technology in downhole slurry flow measurement are analyzed. The test results show that the downhole annular electromagnetic flow measurement based on double-frequency rectangular wave excitation can not only satisfy the requirements of regular electromagnetic flow measurement but also suppress the annular slurry interference effectively.
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N. Salama, A. Bergh, J. E. Damber. "MICROVASCULAR TESTICULAR BLOOD FLOW AS EVALUATED BY LASER DOPPLER FLOWMETRY AFTER THE SURGICAL INDUCTION OF VARICOCELE." Archives of Andrology 46, no. 3 (January 2001): 197–204. http://dx.doi.org/10.1080/01485010151096487.
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Ishimoto, H., M. Natori, M. Tanaka, T. Miyazaki, T. Kobayashi, and Y. Yoshimura. "Role of oxygen-derived free radicals in free growth retardation induced by ischemia-reperfusion in rats." American Journal of Physiology-Heart and Circulatory Physiology 272, no. 2 (February 1, 1997): H701—H705. http://dx.doi.org/10.1152/ajpheart.1997.272.2.h701.
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We investigated the involvement of oxygen-derived free radicals in the pathogenesis of the intrauterine growth retardation (IUGR) induced in Sprague-Dawley rats by ischemia-reperfusion. On day 17 of gestation, rats received saline, superoxide dismutase (SOD, 50,000 U/kg), catalase (CAT, 50,000 U/kg), or SOD + CAT subcutaneously 1 h before induction of 30 min of ischemia of the right uterine horn. On day 21 the placental level of lipid peroxides was significantly increased (P < 0.001 vs. sham-operated group) and IUGR was induced (P < 0.001 vs. left horn) in the saline-treated group n = 6). Pretreatment with SOD + CAT (n = 6) significantly inhibited the increase in placental lipid peroxides and prevented IUGR. The effect of ischemia-reperfusion on uterine blood flow, with or without pretreatment with radical scavengers, was investigated in separate experiments by laser-Doppler flowmetry. The induction of hypoperfusion 3 h after ischemia (blood flow -40 +/- 5%, n = 6, P < 0.05) was blocked by pretreatment with SOD + CAT (n = 6). Results indicate that oxygen-derived free radicals may be important in the development of postischemic uteroplacental hypoperfusion and of ischemia-reperfusion-induced IUGR in the rat.
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Dirnagl, Ulrich, Bruce Kaplan, Michael Jacewicz, and William Pulsinelli. "Continuous Measurement of Cerebral Cortical Blood Flow by Laser—Doppler Flowmetry in a Rat Stroke Model." Journal of Cerebral Blood Flow & Metabolism 9, no. 5 (October 1989): 589–96. http://dx.doi.org/10.1038/jcbfm.1989.84.
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Laser-Doppler flowmetry (LDF), a new method allowing instantaneous, continuous, and noninvasive measurements of microcirculatory blood flow in a small tissue sample, was evaluated for its accuracy in monitoring regional cerebral blood flow (rCBF) in the cortical microcirculation after focal cerebral ischemia. Wistar and spontaneously hypertensive rats (SHR, n = 19) were subjected to permanent occlusion of the middle cerebral and common carotid arteries. Absolute rCBF in a tissue sample of the ischemic hemisphere was measured autoradiographically with [14C]iodoantipyrine as a tracer and compared to rCBF measured by LDF. Additionally, the percent change in rCBF between baseline and ischemic values was compared for both methods. Absolute rCBF values recorded with LDF correlated poorly ( r = 0.54) with [14C]iodoantipyrine measurements. In contrast, LDF readings expressed as a percentage of ischemic vs. preocclusion readings (relative LDF readings) correlated very well ( r = 0.91) with the percent change in [14C]iodoantipyrine measurements. We conclude that LDF does not provide accurate measurements of absolute rCBF values but this method allows accurate measurements of changes in rCBF due to induction of focal cerebral ischemia.
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Westermaier, Thomas, Stefan Zausinger, Alexander Baethmann, Hans-Jakob Steiger, and Robert Schmid-Elsaesser. "No additional neuroprotection provided by barbiturate-induced burst suppression under mild hypothermic conditions in rats subjected to reversible focal ischemia." Journal of Neurosurgery 93, no. 5 (November 2000): 835–44. http://dx.doi.org/10.3171/jns.2000.93.5.0835.
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Object. Mild-to-moderate hypothermia is increasingly used for neuroprotection in humans. However, it is unknown whether administration of barbiturate medications in burst-suppressive doses—the gold standard of neuroprotection during neurovascular procedures—provides an additional protective effect under hypothermic conditions. The authors conducted the present study to answer this question.Methods. Thirty-two Sprague—Dawley rats were subjected to 90 minutes of middle cerebral artery occlusion and randomly assigned to one of four treatment groups: 1) normothermic controls; 2) methohexital treatment (burst suppression); 3) induction of mild hypothermia (33°C); and 4) induction of mild hypothermia plus methohexital treatment (burst suppression). Local cerebral blood flow was continuously monitored using bilateral laser Doppler flowmetry and electroencephalography. Functional deficits were quantified and recorded during daily neurological examinations. Infarct volumes were assessed histologically after 7 days. Methohexital treatment, mild hypothermia, and mild hypothermia plus methohexital treatment reduced infarct volumes by 32%, 71%, and 66%, respectively, compared with normothermic controls. Furthermore, mild hypothermia therapy provided the best functional outcome, which was not improved by additional barbiturate therapy.Conclusions. The results of this study indicate that barbiturate-induced burst suppression is not required to achieve maximum neuroprotection under mild hypothermic conditions. The magnitude of protection afforded by barbiturates alone appears to be modest compared with that provided by mild hypothermia.
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Busch, Hans-Jörg, Ivo R. Buschmann, Günter Mies, Christoph Bode, and Konstantin-Alexander Hossmann. "Arteriogenesis in Hypoperfused Rat Brain." Journal of Cerebral Blood Flow & Metabolism 23, no. 5 (May 2003): 621–28. http://dx.doi.org/10.1097/01.wcb.0000057741.00152.e4.
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Experimental and clinical studies have provided evidence for spontaneous and therapeutically induced arteriogenesis after occlusion of major peripheral or cardiac vessels. Such evidence is lacking for the cerebrovascular system. In halothane-anesthetized rats, different degrees of brain hypoperfusion were induced by one- to four-vessel occlusion, that is, one or both common carotid arteries in combination with or without bilateral vertebral artery occlusion. The flow decline was monitored by laser Doppler flowmetry, the residual hemodynamic reserve by testing flow reactivity to ventilation with 6% CO2 and arteriogenesis by intravascular latex infusion and immunohistochemistry of vascular proliferation and monocyte adhesion. The optimum condition for induction of arteriogenesis was three-vessel (one carotid plus both vertebral arteries) occlusion, which led to reduction of blood flow to about 50% and complete suppression of CO2 reactivity, but no histologic injury. One week after three-vessel occlusion, the ipsilateral posterior cerebral artery significantly enlarged by 39%, and after 3 weeks by 72%, paralleled by the partial return of CO2 reactivity and the appearance of immunohistochemical markers of arteriogenesis. Three-vessel occlusion is a reliable model for the induction of arteriogenesis in the adult brain and is a new approach for exploring the potentials of arteriogenesis for the prevention of progressing brain ischemia.
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Sakurada, S., O. Shido, K. Yamamoto, N. Sugimoto, T. Kobayashi, and T. Nagasaka. "Effect of digital nerve blockade on heat-induced vasoconstriction in the human finger." Journal of Applied Physiology 78, no. 2 (February 1, 1995): 746–49. http://dx.doi.org/10.1152/jappl.1995.78.2.746.
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The present study was performed to investigate the mechanism of heat-induced vasoconstriction (HIVC) in human fingers. The left fingers of five male subjects were immersed in water controlled at an initial temperature of 35.0 degrees C. The blood flows (BF) of the left index and fourth fingers were measured continuously with laser-Doppler flowmeter probes, and the temperatures of the middle finger and water bath were also monitored continuously using thermistor probes. Arterial blood pressure and heart rate were measured every minute before and during local finger warming. A local anesthetic (0.5% bupivacaine hydrochloride) or saline at a volume of 5.0–8.0 ml was aseptically injected into the base of the fourth or index finger, respectively. After finger BFs had been stabilized for > or = 10 min, the fingers were warmed by raising the water bath temperature from 35.0 to 41.5 degrees C in 14 min. The BF of the index finger fell significantly for 6 min after local warming was commenced (at water bath temperatures between 35.5 and 37.5 degrees C) without associated changes in mean arterial blood pressure, indicating the occurrence of HIVC. Then BF increased toward prewarming levels. The local anesthetic injection, however, completely abolished HIVC in the fourth finger. These results suggest that, in humans, innervation to finger vessels is indispensable for producing HIVC and hence that a local mechanism, such as myogenic vascular response to high temperature, may not be involved in the induction of HIVC.
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Karibe, Hiroshi, Jun Chen, Gregory J. Zarow, Steven H. Graham, and Philip R. Weinstein. "Delayed induction of mild hypothermia to reduce infarct volume after temporary middle cerebral artery occlusion in rats." Journal of Neurosurgery 80, no. 1 (January 1994): 112–19. http://dx.doi.org/10.3171/jns.1994.80.1.0112.
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✓ Deep to moderate hypothermia (24° to 30°C) during focal cerebral ischemia reduces infarct volume but must be initiated before the onset of ischemia to be effective and has deleterious pulmonary, myocardial and neurological effects. It is not known whether mild hypothermia (32° to 33°C) protects against ischemic neuronal damage, whether hypothermia induced after the onset of ischemia has protective effects, or whether these effects are associated with alterations in cortical blood flow. In this study, mild whole-body hypothermia was induced in rats just before or 10, 30, or 60 minutes after the onset of 2 hours of temporary middle cerebral artery occlusion; rewarming began immediately after reversal of occlusion and normothermia was maintained throughout 22 hours of reperfusion. Infarct volume, measured 24 hours after the end of reperfusion, was significantly smaller in rats made hypothermic within 30 minutes after the onset of ischemia than in normothermic controls; hypothermia induced at 60 minutes of ischemia did not reduce infarct volume. Cortical blood flow, measured by laser Doppler ultrasound flowmetry, was not significantly different between groups during ischemia; however, postischemic cortical blood flow correlated positively with total infarct volume. These results indicate that mild hypothermia initiated during temporary focal ischemia in rats can reduce infarct volume without attenuating the reduction in cortical blood flow.
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Wallace, J. L., C. M. Hogaboam, and G. W. McKnight. "Platelet-activating factor mediates gastric damage induced by hemorrhagic shock." American Journal of Physiology-Gastrointestinal and Liver Physiology 259, no. 1 (July 1, 1990): G140—G146. http://dx.doi.org/10.1152/ajpgi.1990.259.1.g140.
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The role of platelet-activating factor (PAF) as a mediator of the gastric damage associated with hemorrhagic shock was investigated using a rat model. With use of an ex vivo gastric chamber preparation, the gastric mucosa was bathed with 0.1 M HCl for 90 min. At minute 10 the systemic arterial blood pressure (BP) was reduced to 25 mmHg by bleeding from the femoral artery. BP was maintained at this level for 15 min, then the shed blood was reinfused. In control rats subjected to this protocol, extensive gastric damage developed during and after the shock period and involved an average of 50 +/- 8% of the total area of glandular mucosa. A marked decrease in transmucosal potential difference (PD) was observed during shock, with little recovery thereafter. Also, significant appearance of protein and hemoglobin (Hb) in the gastric lumen was detected after induction of shock. Oral pretreatment of the rats with the PAF antagonist WEB 2086 (0.5-20 mg/kg) dose dependently reduced the extent of macroscopically visible gastric damage, the decrease in transmucosal PD, and the appearance in the lumen of protein and Hb. A similar protective effect was observed with another PAF antagonist, BN 52021 (10 mg/kg). With use of laser-Doppler flowmetry, changes in gastric blood flow were determined before, during, and after induction of shock.(ABSTRACT TRUNCATED AT 250 WORDS)
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Shoji, Tetsuya, Yoshikazu Yonemitsu, Kimihiro Komori, Mitsugu Tanii, Hiroyuki Itoh, Shihoko Sata, Hiroaki Shimokawa, Mamoru Hasegawa, Katsuo Sueishi, and Yoshihiko Maehara. "Intramuscular gene transfer of FGF-2 attenuates endothelial dysfunction and inhibits intimal hyperplasia of vein grafts in poor-runoff limbs of rabbit." American Journal of Physiology-Heart and Circulatory Physiology 285, no. 1 (July 2003): H173—H182. http://dx.doi.org/10.1152/ajpheart.00996.2002.
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We previously demonstrated that sustained disturbance of endothelium-dependent vasorelaxation and poor distal runoff in ischemic limbs were critical factors affecting the neointimal development of autologous vein grafts (VGs). Also, we recently showed the superior therapeutic potential of basic fibroblast growth factor (bFGF/FGF-2) boosted by the recombinant Sendai virus (SeV) for severe limb ischemia compared with that of vascular endothelial growth factor. Here, the effect of FGF-2 on neointimal hyperplasia of VGs was examined in a rabbit model of poor-runoff limbs. Two weeks after initial surgery for the induction of poor-runoff, SeV-expressing human FGF-2 (SeV-hFGF2) or that encoding firefly luciferase (109 plaque-forming units/head) was injected into the thigh and calf muscle. At that time, the femoral vein was implanted in the femoral artery in an end-to-end manner in some groups. FGF-2 gene-transferred limbs demonstrated significantly increased blood flow assessed not only by laser Doppler flow image but also by ultrasonic transit-time flowmeter (USTF). USTF also showed a significant increase in the blood flow ratio of the deep femoral artery to external iliac artery, indicating that collateral flow was significantly restored in the thigh muscles ( P < 0.01). Reduction of neointimal hyperplasia was also observed in the VGs treated by SeV-hFGF2; these grafts demonstrated significant restoration of endothelium-dependent vasorelaxation. These findings thus extend the indications of therapeutic angiogenesis using SeV-hFGF2 to include not only limb salvage but also prevention of late graft failure.
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Shimoda, Osamu, Yoshihiro Ikuta, Masakatsu Sakamoto, and Hidenori Terasaki. "Skin Vasomotor Reflex Predicts Circulatory Responses to Laryngoscopy and Intubation." Anesthesiology 88, no. 2 (February 1, 1998): 297–304. http://dx.doi.org/10.1097/00000542-199802000-00005.
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Background An evaluation of autonomic reactivity may help to predict circulatory responses to intubation. The relation between the magnitude of the skin vasomotor reflex (SVmR) immediately before laryngoscopy and the circulatory responses to intubation was examined. Methods Forty-four adult patients (classified as American Society of Anesthesiologists physical status I or II) were studied. General anesthesia was induced with fentanyl and thiamylal and maintained with nitrous oxide and sevoflurane. The SVmR was evoked by an electrostimulus to the ulnar nerve, and decreases in skin blood flow were detected using a laser-Doppler flowmeter. In study 1, two groups of patients were studied. In the monitored group (n = 14), laryngoscopy was performed when the SVmR amplitude had decreased to less than 0.1. In the control group (n = 15), intubation was performed regardless of changes in the SVmR amplitude. In study 2, after induction, the end-tidal concentration of sevoflurane was maintained at 1 MAC (n = 9) or 1.3 MAC (n = 6) for 5 min. The SVmR was tested by changing the electric intensity. Results In study 1, the blood pressure and heart rate of the control group increased significantly (P < 0.01) after laryngoscopy. The blood pressure of the monitored group did not increase. The SVmR amplitude and the systolic blood pressure changes showed a significant linear correlation (P < 0.001). In study 2, the relation between the electric intensity and the SVmR amplitude showed a weak but significant correlation (P < 0.01) in the 1 MAC group. Conclusion The evaluation of the SVmR provides useful information for determining the optimal anesthetic depth for laryngoscopy and intubation in individual patients.
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Poynton-Smith, E., E. Colwill, and O. Sahota. "79 Do Medical Students Understand the Ward Environment? A Survey of Penultimate Year Medical Students Exploring How Well Healthcare Of Older People Placements Prepare Them for Working on Hospital Wards." Age and Ageing 49, Supplement_1 (February 2020): i25—i26. http://dx.doi.org/10.1093/ageing/afz191.04.
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Abstract Medical students are expected to know how to function on hospital wards; i.e. where to find things, other Health Care Professionals’ (HCPs’) roles, and how to use certain items of equipment (GMC, 2018). This ward-based knowledge indicates that a student is ‘ward smart’.1 Whilst being ‘ward smart’ is key for many aspects of medicine, it is particularly important for students learning geriatric medicine: older patients (who make up around 42% of all inpatients)2 are more likely to have communication difficulties and to require assistance. However, formal teaching in this area seems to be somewhat neglected, with students being left to ‘pick up’ this knowledge as they go along.3,4 In our sample of 41 students in their penultimate year (most of whom were undertaking their Healthcare of Older People placement), 98% did not know how to turn on a hearing aid and only 24% knew what a Waterlow score was. Furthermore, 88% did not know how to read an oxygen flowmeter, and only 59% knew where the CPR lever on the bed was situated. This is a significant gap in knowledge: Students may not be as prepared to work in a ward environment as expected. Students felt that their understanding would be improved by teaching sessions, more time on wards, formal ward inductions, and shadowing other HCPs: only 41.5% had had a ward induction or introduction, and less than 20% had shadowed a nurse. We propose specific teaching/practical sessions for students during their Healthcare of Older People placement centred around patient communication and understanding the ward environment. References 1. Walker, Wallace, Mangera, & Gill, The Clinical Teacher, 2017, 14(5), 336–9. 2. NHS Digital, 2018. 3. Prince, Bozhuizen, Van der Vleuten, & Scherpbier, Medical Education 2005; 39(7):704–12. 4. Monrouxe, et al., BMJ Open 2017; 7(1):e013656.
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Hertelendy, Péter, Ákos Menyhárt, Péter Makra, Zoltán Süle, Tamás Kiss, Gergely Tóth, Orsolya Ivánkovits-Kiss, Ferenc Bari, and Eszter Farkas. "Advancing age and ischemia elevate the electric threshold to elicit spreading depolarization in the cerebral cortex of young adult rats." Journal of Cerebral Blood Flow & Metabolism 37, no. 5 (July 20, 2016): 1763–75. http://dx.doi.org/10.1177/0271678x16643735.
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Spreading depolarizations of long cumulative duration have been implicated in lesion development and progression in patients with stroke and traumatic brain injury. Spreading depolarizations evolve less likely in the aged brain, but it remains to be determined at what age the susceptibility to spreading depolarizations starts to decline, especially in ischemia. Spreading depolarizations were triggered by epidural electric stimulation prior and after ischemia induction in the cortex of 7–30 weeks old anesthetized rats ( n = 38). Cerebral ischemia was achieved by occlusion of both common carotid arteries. Spreading depolarization occurrence was confirmed by the acquisition of DC potential and electrocorticogram. Cerebral blood flow variations were recorded by laser-Doppler flowmetry. Dendritic spine density in the cortex was determined in Golgi-COX stained sections. Spreading depolarization initiation required increasingly greater electric charge with older age, a potential outcome of consolidation of cortical connections, indicated by altered dendritic spine distribution. The threshold of spreading depolarization elicitation increased with ischemia in all age groups, which may be caused by tissue acidosis and increased K+ conductance, among other factors. In conclusion, the brain appears to be the most susceptible to spreading depolarizations at adolescent age; therefore, spreading depolarizations may occur in young patients of ischemic or traumatic brain injury at the highest probability.
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Savitz, Sean I., Joseph A. Erhardt, James V. Anthony, Gaurav Gupta, Xiang Li, Frank C. Barone, and Daniel M. Rosenbaum. "The Novel β-Blocker, Carvedilol, Provides Neuroprotection in Transient Focal Stroke." Journal of Cerebral Blood Flow & Metabolism 20, no. 8 (August 2000): 1197–204. http://dx.doi.org/10.1097/00004647-200008000-00005.
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Increasing evidence supports a role for oxidative stress, proinflammatory cytokines, and apoptosis in the pathophysiology of focal ischemic stroke. Previous studies have found that the multi-action drug, carvedilol, is a mixed adrenergic antagonist, and that it behaves as an antioxidant and inhibits apoptosis. In the current study, the authors investigated whether carvedilol provides protection in focal cerebral ischemia and whether this protection is associated with reduced apoptosis and the downregulation of the inflammatory cytokines, tumor necrosis factor-α (TNF-α) and interleukin-1β (IL-1β). Male Sprague-Dawley rats were subjected to transient middle cerebral artery occlusion (MCAO) by an intraluminal filament technique. Carvedilol (1, 3, and 10 mg/kg) was injected daily subcutaneously 2 or 4 days before the induction of ischemia. Neurologic scores, infarct volumes, TUNEL staining, and mRNA levels of TNF-α and IL-Iβ were assessed at 24 hours reperfusion. The effect of carvedilol on microvascular cortical perfusion was studied with continuous laser—Doppler flowmetry. Twenty-four hours after MCAO, carvedilol at all three doses reduced infarct volumes by at least 40% and reduced neurologic deficits on average by 40% compared with vehicle-treated controls when given 2 or 4 days before the induction of ischemia. This protection was not mediated by changes in temperature or blood flow. Treatment with all three dose regimens resulted in fewer TUNEL positive cells compared with controls. At 24 hours reperfusion, carvedilol decreased TNF-α and IL-1β expression by 40% to 50% in the ipsilateral ischemic cortex compared with the contralateral controls. The results of the current study indicate that carvedilol is neuroprotective in focal cerebral ischemia and may protect the ischemic brain by inhibiting apoptosis and attenuating the expression of TNF-α and IL-1β.
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Westermaier, Thomas, Alina Jauss, Jörg Eriskat, Ekkehard Kunze, and Klaus Roosen. "Acute vasoconstriction: decrease and recovery of cerebral blood flow after various intensities of experimental subarachnoid hemorrhage in rats." Journal of Neurosurgery 110, no. 5 (May 2009): 996–1002. http://dx.doi.org/10.3171/2008.8.jns08591.
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Object Immediate vasoconstriction after subarachnoid hemorrhage (SAH) has been observed in a number of experimental studies. However, it has not yet been examined which pattern this acute-type vascular reaction follows and whether it correlates with the intensity of SAH. It was the purpose of the present study to vary the extent of SAH using the endovascular filament model of SAH with increasing filament sizes and to compare the course of intracranial pressure (ICP), cerebral perfusion pressure (CPP), and regional cerebral blood flow (rCBF). Methods Male Sprague-Dawley rats were subjected to SAH using the endovascular filament model. Subarachnoid hemorrhage was induced using a 3-0, 4-0, or 5-0 Prolene monofilament (8 rats in each group). Eight animals served as controls. Bilateral rCBF (laser Doppler flowmetry), mean arterial blood pressure, and ICP were continuously monitored. Thereafter, the rats were allowed to wake up. Twenty-four hours later, the animals were killed, their brains were removed, and the extent of SAH was determined. Results After induction of SAH, ICP steeply increased while CPP and rCBF rapidly declined in all groups. With increasing size of the filament, the increase of ICP and the decrease of CPP were more pronounced. However, the decline of rCBF exceeded the decline of CPP in all SAH groups. In a number of animals with minor SAH, an oscillating pattern of rCBF was observed during induction of SAH and during early recovery. Conclusions The disparity between the decline and recovery of CPP and rCBF suggests that acute vasoconstriction occurs even in SAH of a minor extent. Acute vasoconstriction may contribute significantly to a perfusion deficit in the acute stage after SAH. The oscillating pattern of rCBF in the period of early recovery after SAH resembles the pattern of synchronized vasomotion, which has been thoroughly examined for other vascular territories and may yield therapeutic potential.
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Hamming, Arend M., Marieke JH Wermer, S. Umesh Rudrapatna, Christian Lanier, Hine JA van Os, Walter M. van den Bergh, Michel D. Ferrari, et al. "Spreading depolarizations increase delayed brain injury in a rat model of subarachnoid hemorrhage." Journal of Cerebral Blood Flow & Metabolism 36, no. 7 (November 30, 2015): 1224–31. http://dx.doi.org/10.1177/0271678x15619189.
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Spreading depolarizations may contribute to delayed cerebral ischemia after aneurysmal subarachnoid hemorrhage, but the effect of spreading depolarizations on brain lesion progression after subarachnoid hemorrhage has not yet been assessed directly. Therefore, we tested the hypothesis that artificially induced spreading depolarizations increase brain tissue damage in a rat model of subarachnoid hemorrhage. Subarachnoid hemorrhage was induced by endovascular puncture of the right internal carotid bifurcation. After one day, brain tissue damage was measured with T2-weighted MRI, followed by application of 1 M KCl (SD group, N = 16) or saline (no-SD group, N = 16) to the right cortex. Cortical laser-Doppler flowmetry was performed to record spreading depolarizations. MRI was repeated on day 3, after which brains were extracted for assessment of subarachnoid hemorrhage severity and histological damage. 5.0 ± 2.7 spreading depolarizations were recorded in the SD group. Subarachnoid hemorrhage severity and mortality were similar between the SD and no-SD groups. Subarachnoid hemorrhage-induced brain lesions expanded between days 1 and 3. This lesion growth was larger in the SD group (241 ± 233 mm3) than in the no-SD group (29 ± 54 mm3) (p = 0.001). We conclude that induction of spreading depolarizations significantly advances lesion growth after experimental subarachnoid hemorrhage. Our study underscores the pathophysiological consequence of spreading depolarizations in the development of delayed cerebral tissue injury after subarachnoid hemorrhage.
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Kehl, Franz, Liana Cambj-Sapunar, Kristopher G. Maier, Noriyuki Miyata, Shunishi Kametani, Hirotsugu Okamoto, Anthony G. Hudetz, et al. "20-HETE contributes to the acute fall in cerebral blood flow after subarachnoid hemorrhage in the rat." American Journal of Physiology-Heart and Circulatory Physiology 282, no. 4 (April 1, 2002): H1556—H1565. http://dx.doi.org/10.1152/ajpheart.00924.2001.
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This study examined the effects of blocking the formation of 20-hydroxyeicosatetraenoic acid (20-HETE) on the acute fall in cerebral blood flow after subarachnoid hemorrhage (SAH) in the rat. In vehicle-treated rats, regional cerebral blood flow (rCBF) measured with laser-Doppler flowmetry fell by 30% 10 min after the injection of 0.3 ml of arterial blood into the cisterna magna, and it remained at this level for 2 h. Pretreatment with inhibitors of the formation of 20-HETE, 17-octadecynoic acid (17-ODYA; 1.5 nmol intrathecally) and N-hydroxy- N′-(4-butyl-2-methylphenyl)formamidine (HET0016; 10 mg/kg iv), reduced the initial fall in rCBF by 40%, and rCBF fully recovered 1 h after induction of SAH. The concentration of 20-HETE in the cerebrospinal fluid rose from 12 ± 2 to 199 ± 17 ng/ml after SAH in vehicle-treated rats. 20-HETE levels averaged only 15 ± 11 and 39 ± 13 ng/ml in rats pretreated with 17-ODYA or HET0016, respectively. HET0016 selectively inhibited the formation of 20-HETE in rat renal microsomes with an IC50of <15 nM and human recombinant CYP4A11, CYP4F2, and CYP4F3 enzymes with an IC50 of 42, 125, and 100 nM, respectively. These results indicate that 20-HETE contributes to the acute fall in rCBF after SAH in rats.
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Nawashiro, Hiroshi, Michael Brenner, Shinji Fukui, Katsuji Shima, and John M. Hallenbeck. "High Susceptibility to Cerebral Ischemia in GFAP-Null Mice." Journal of Cerebral Blood Flow & Metabolism 20, no. 7 (July 2000): 1040–44. http://dx.doi.org/10.1097/00004647-200007000-00003.
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Astrocytes perform a variety of functions in the adult central nervous system (CNS) that contribute to the survival of neurons. Thus, it is likely that the activities of astrocytes affect the extent of brain damage after ischemic stroke. The authors tested this hypothesis by using a mouse ischemia model to compare the infarct volume produced in wild-type mice with that produced in mice lacking glial fibrillary acidic protein (GFAP), an astrocyte specific intermediate filament component. Astrocytes lacking GFAP have been shown to have defects in process formation, induction of the blood-brain barrier, and volume regulation; therefore, they might be compromised in their ability to protect the CNS after injury. The authors reported here that 48 hours after combined permanent middle cerebral artery occlusion (MCAO) and 15 minutes transient carotid artery occlusion (CAO) GFAP-null mice had a significantly ( P < 0.001) larger cortical infarct volume (16.7 ± 2.2 mm3) than their wild-type littermates (10.1 ± 3.9 mm3). Laser-Doppler flowmetry revealed that the GFAP-null mice had a more extensive and profound decrease in cortical cerebral blood flow within 2 minutes after MCAO with CAO. These results indicated a high susceptibility to cerebral ischemia in GFAP-null mice and suggested an important role for astrocytes and GFAP in the progress of ischemic brain damage after focal cerebral ischemia with partial reperfusion.
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Goadsby, Peter J., Mikael Adner, and Lars Edvinsson. "Characterization of Endothelin Receptors in the Cerebral Vasculature and Their Lack of Effect on Spreading Depression." Journal of Cerebral Blood Flow & Metabolism 16, no. 4 (July 1996): 698–704. http://dx.doi.org/10.1097/00004647-199607000-00021.
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The changes in cerebral blood flow that accompany spreading depression are well-described, as are parallel changes in cellular activity, with a wave of hyperemia followed by a prolonged oligemic phase. In this study, a cat model of the CBF changes associated with spreading depression and in vitro pharmacology were used to determine if there is a role for the powerful peptide vasoconstrictor endothelin in this response. For the pharmacological studies, the middle cerebral artery was harvested from cats postmortem. For the physiological studies, cats were anesthetized with halothane induction and α-chloralose (60 mg/kg, intraperitoneal loading; 20 mg/kg i.v. 2-h maintenance). CBF was monitored continuously in the parietal cortex using laser Doppler flowmetry (CBFLDF) after exposure of the dura mater. The in vitro work demonstrated that endothelin-1 (ET-1) mediates a strong and potent contraction of cerebral vessels. Both the selective ETA receptor antagonist FR139317 and the combined ETA and ETB receptor antagonist Bosentan caused a rightward shift of the concentration-response curve without attenuation of the maximum effect. The calculated pA2 values were 6.28 and 6.90, respectively. The slope did not differ from unity, suggesting that the ET-1-mediated contraction is evoked by a single population of ETA receptors, which were effectively antagonized by these compounds. Spreading depression was induced with a needle stick injury to the cortex. Local administration of the endothelin antagonists FR139317 (10 μ M) and Bosentan (10 μ M) did not affect resting blood flow in the cortex. Induction of spreading depression following local administration of FR139317 and Bosentan resulted in responses no different from those in control cortex. These data demonstrate that endothelin does not play a significant role in the vasoconstrictor portion of the CBF change seen in spreading depression, nor does it affect resting flow. Since it is widely held that spreading depression, or a very similar mechanism, underlies the aura phase of migraine, it may be suggested from these studies that endothelin antagonists are unlikely to be useful in migraine.
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Freret, Thomas, Valentine Bouet, Jérôme Toutain, Romaric Saulnier, Palma Pro-Sistiaga, Ebeline Bihel, Eric T. MacKenzie, Simon Roussel, Pascale Schumann-Bard, and Omar Touzani. "Intraluminal Thread Model of Focal Stroke in the Non-Human Primate." Journal of Cerebral Blood Flow & Metabolism 28, no. 4 (November 14, 2007): 786–96. http://dx.doi.org/10.1038/sj.jcbfm.9600575.
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The common marmoset ( Callithrix jacchus), a New World monkey, has recently been used as a model of focal cerebral ischaemia. Here, we sought to develop a stroke model in this species using an intraluminal approach to occlude the middle cerebral artery (MCA). This technically simple procedure allows both transient and permanent ischaemia with minimal morbidity. Ten common marmosets underwent either transient (3 h) or permanent ischaemia by the insertion of a nylon filament through the external carotid artery up to the origin of the MCA. Cerebral blood flow (CBF) was monitored by the laser-Doppler flowmetry technique. Sensorimotor functions were regularly evaluated, and histologic, immunohistochemical, and magnetic resonance imaging analyses were performed 8 days after the occlusion. The surgical procedure was achieved straightforwardly without postoperative mortality or cerebral haemorrhage. All animals displayed a consistent decrease in CBF that remained stable over 3 h. Infarction affected both cortical and subcortical structures. Although not statistically significant, the volume of infarction was smaller in marmosets subjected to transient ischaemia compared to those permanently occluded (237±139 and 358±118 mm3, respectively). In all the behavioural tests used, reperfused marmosets exhibited fewer neurologic and functional impairments compared to permanently occluded ones. We show the feasibility of the induction of permanent or transient focal cerebral ischaemia in the marmoset using an intraluminal approach with minimal invasion. This model could be suitable as an advanced screening for potential stroke therapies in which behavioural, imaging, and histologic analyses can be compared.
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Iadecola, C., F. Zhang, and X. Xu. "Inhibition of inducible nitric oxide synthase ameliorates cerebral ischemic damage." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 268, no. 1 (January 1, 1995): R286—R292. http://dx.doi.org/10.1152/ajpregu.1995.268.1.r286.
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We sought to determine whether expression of the inducible, calcium-independent isoform of nitric oxide synthase (iNOS) contributes to the tissue damage produced by focal cerebral ischemia. The middle cerebral artery was occluded in halothane-anesthetized spontaneously hypertensive rats. Twenty-four hours later rats received intraperitoneal injections of the iNOS inhibitor aminoguanidine (100 mg/kg twice per day; n = 10) or of aminoguanidine + L-arginine (300 mg/kg four times per day; n = 7), aminoguanidine + D-arginine (n = 7), arginine alone (n = 6), or vehicle (n = 9). Drugs were administered for 3 consecutive days. Infarct volume was determined by image analysis in thionin-stained brain sections 4 days after induction of ischemia. Administration of aminoguanidine reduced infarct volume by 33 +/- 4% (P < 0.05 from vehicle; analysis of variance and Tukey's test), a reduction that was antagonized by coadministration of L- but not D-arginine. Administration of L-arginine alone did not affect infarct size (P > 0.05 vs. vehicle). In separate rats (n = 10), aminoguanidine attenuated calcium-independent NOS activity in the infarct (P < 0.05 vs. vehicle) without affecting calcium-dependent activity (P > 0.05). Aminoguanidine did not affect resting cerebral blood flow or the cerebrovascular vasodilation elicited by hypercapnia, as determined by laser-Doppler flowmetry (n = 4). We conclude that aminoguanidine selectively inhibits iNOS activity in the area of infarction and reduces the volume of the infarct produced by middle cerebral artery occlusion.(ABSTRACT TRUNCATED AT 250 WORDS)
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Assadi, Abdelnasser, Olivier Desebbe, Thomas Rimmelé, Arnal Florence, Joëlle Goudable, Dominique Chassard, and Bernard Allaouchiche. "Small-volume hypertonic saline/pentastarch improves ileal mucosal microcirculation in experimental peritonitis." Infectious Disease Reports 4, no. 1 (March 5, 2012): 22. http://dx.doi.org/10.4081/idr.2012.e22.
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We compared the effects of hypertonic saline 7.2% / 6% hydroxyethyl starch (HSS-HES) and isotonic saline 0.9% / 6% hydroxyethyl starch (ISS-HES) on ileal microcirculatory blood flow (MBF) at the initial phase of septic shock. Pigs were anesthetized and mechanically ventilated. Catheters were inserted into right atrium, pulmonary artery, carotid artery, and portal vein for hemodynamic measurements and for blood sampling. Ileal mucosal and muscularis MBF was continuously measured by laser Doppler flowmetry (LDF). Septic shock was obtained 240 min after induction of fecal peritonitis; then animals were randomized to receive 10 mL.kg-1 during 10 min of either HSS-HES or ISS-HES. Systemic and microcirculatory blood flow as well as systemic metabolism were assessed. Fecal peritonitis promoted a hypodynamic septic shock, with significant reduction of mean arterial pressure (MAP) and cardiac index (CI). Ileal mucosal MBF (-34%) and ileal muscularis MBF (-54%) significantly diminished from baseline. Contrary to ISS-HES group, mucosal MBF significantly augmented after HSS-HES (+192% at min 150 post-shock) despite low blood pressure. There was weak correlation with CI (r²= 0.2, P = 0.01) . Muscularis MBF didn’t change. HSS-HES-treated animals had a significantly higher osmolarity and sodium concentration than ISS-HES group. Other variables did not change. Small-volume resuscitation with HSS-HES, but not ISS-HES, improved ileal microcirculatory impairment in experimental peritonitis model of septic shock even when MAP was low. This beneficial microcirculatory effect could be valuable in the management of early severe sepsis.
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Zhang, Zhenggang, Rui Lan Zhang, Quan Jiang, Sundara B. K. Raman, Lois Cantwell, and Michael Chopp. "A New Rat Model of Thrombotic Focal Cerebral Ischemia." Journal of Cerebral Blood Flow & Metabolism 17, no. 2 (February 1997): 123–35. http://dx.doi.org/10.1097/00004647-199702000-00001.
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We developed a fibrin-rich thrombotic focal cerebral ischemic model with reproducible and predictable infarct volume in rats. In male Wistar rats (n = 77), a thrombus was induced at the origin of the middle cerebral artery (MCA) by injection of thrombin via an intraluminal catheter placed in the intracranial segment of the internal carotid artery (ICA). Thrombus induction and consequent ischemic cell damage were examined by histopathological analysis and neurological deficit scoring, and by measuring changes in cerebral blood flow (CBF) using laser–Doppler flowmetery (LDF), perfusion-weighted imaging (PWI), and by diffusion weighted imaging (DWI). Histopathology revealed that a fibrin-rich thrombus localized to the origin of the right MCA. Regional cerebral blood flow (rCBF) in the right parietal cortex was reduced by 34–58% of preinjection levels after injection of thrombin in rats administered 30 U of thrombin (n = 10). Magnetic resonance imaging (MRI) showed a reduction in CBF and a hyperintensity DWI encompassing the territory supplied by the right MCA. The infarct volume in rats administered 80 U of thrombin was 31.29 ± 12.9% of the contralateral hemisphere at 24 h (n = 13), and 34.7 ± 16.4% of the contralateral hemisphere at 168 h (n = 6). Rats administered 30 U of thrombin exhibited a hemispheric infarct volume of 34.0 ± 14.5% (n = 9) at 24 h and 29.7 ± 13.9% (n = 8) at 168 h. In addition, thrombotic rats (n = 3) treated with recombinant tissue plasminogen activator (rt-PA) (10 mg/kg) 2 h after thrombosis showed that CBF rapidly returned towards preischemic values as measured by PWI. This model of thrombotic ischemia is relevant to thromboembolic stroke in humans and may be useful in documenting the safety and efficacy of thrombolytic intervention as well as for investigating therapies complementary to antithrombotic therapy.
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Takeuchi, Kazuhiko, Marija Renic, Quinn C. Bohman, David R. Harder, Noriyuki Miyata, and Richard J. Roman. "Reversal of delayed vasospasm by an inhibitor of the synthesis of 20-HETE." American Journal of Physiology-Heart and Circulatory Physiology 289, no. 5 (November 2005): H2203—H2211. http://dx.doi.org/10.1152/ajpheart.00556.2005.
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This study characterized the time course of changes in cerebral blood flow (CBF) and vascular diameter in a dual-hemorrhage model of subarachnoid hemorrhage (SAH) in rats and examined whether acute blockade of the synthesis of 20-hydroxyeicosatetraenoic acid (20-HETE) with N-(3-chloro-4-morpholin-4-yl)phenyl- N′-hydroxyimido formamide (TS-011) can reverse delayed vasospasm in this model. Rats received an intracisternal injection of blood (0.4 ml) on day 0 and a second injection 2 days later. CBF was sequentially measured using laser-Doppler flowmetry, and the diameters of the cerebral arteries were determined after filling the cerebral vasculature with a casting compound. CBF fell to 67% of control after the first intracisternal injection of blood but returned to a value near control 24 h later. CBF again fell to 63% of control after a second intracisternal injection of blood and remained 30% below control for 5 days. The fall in CBF after the second intracisternal injection of blood was associated with a sustained 30% reduction in the diameters of the middle cerebral, posterior communicating, and basilar arteries. Acute blockade of the synthesis of 20-HETE with TS-011 (0.1 mg/kg iv), 5 days after the second SAH, increased the diameters of the cerebral arteries, and CBF returned to control. These results indicate that the rats develop delayed vasospasm after induction of the dual-hemorrhage model of SAH and that blockade of the synthesis of 20-HETE fully reverses cerebral vasospasm in this model. They also implicate 20-HETE in the development and maintenance of delayed cerebral vasospasm.
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Schubert, Gerrit A., Lothar Schilling, and Claudius Thomé. "Clazosentan, an endothelin receptor antagonist, prevents early hypoperfusion during the acute phase of massive experimental subarachnoid hemorrhage: a laser Doppler flowmetry study in rats." Journal of Neurosurgery 109, no. 6 (December 2008): 1134–40. http://dx.doi.org/10.3171/jns.2008.109.12.1134.
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Object Acute cerebral hypoperfusion and early disturbances in cerebral autoregulation after subarachnoid hemorrhage (SAH) have been demonstrated repeatedly and have been shown to contribute significantly to acute and secondary brain injury. Acute vasoconstriction has been identified as a major contributing factor. Although increasing evidence implicates endothelin (ET)–1 in the development of cerebral vasospasm, its role in the acute phase after SAH has not yet been investigated. The purpose of this study was to further determine the role of ET in the first minutes to hours after massive experimental SAH induced by prophylactic treatment with the ET receptor antagonist clazosentan. Methods Subarachnoid hemorrhage was induced in 22 anesthetized rats by injection of 0.5-ml arterial, nonheparinized blood into the cisterna magna over the course of 60 seconds. In addition to monitoring intracranial pressure (ICP) and mean arterial blood pressure, laser Doppler flowmetry (LDF) probes were placed stereotactically over the cranial windows to allow online recording of cerebral blood flow (CBF) starting 30 minutes prior to SAH and continuing for 3 hours after SAH. The control group (Group A, 11 rats) received vehicle saline solution via a femoral catheter before SAH, and a second group (Group B, 11 rats) was treated prophylactically with clazosentan, an ETA receptor antagonist. Treatment was started 30 minutes prior to bolus injection (1 mg/kg body weight), immediately followed by a continuous infusion of 1 mg/kg body weight/hr until the end of the experiment. Results Induction of SAH in the rats caused an immediate increase in ICP, which led to an acute decrease in cerebral perfusion pressure (CPP). Perfusion, as measured with LDF, was found to have decreased relative to baseline by 30 ±20% in the control group and 20 ±9% in the clazosentan-treated group. Intracranial pressure and CPP recovered comparably in both groups thereafter within minutes. Control animals demonstrated prolonged hypoperfusion with a loss of autoregulation independent of CPP changes, finally approaching 80% of baseline values toward the end of the experiment. The authors observed that clazosentan did not influence peracute CPP-dependent hypoperfusion, but prevented continuous CBF reduction. Laser Doppler flowmetry perfusion readings remained depressed in control animals at 73 ±19% of baseline in comparison with 106 ±25% of baseline in clazosentan-treated animals (p = 0.001). Conclusions The first hours after a massive experimental SAH can be characterized by a CPP-independent compromise in cerebral perfusion. Prophylactic treatment with the ET receptor antagonist clazosentan prevented hypoperfusion. It is known that in the first days after SAH, a reduction in CBF correlates clinically to high-grade SAH. Although research currently focuses on delayed vasospasm, administration of vasoactive drugs in the acute phase of SAH may reverse perfusion deficits and improve patient recovery.
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Braun, Rod D., Jennifer L. Lanzen, and Mark W. Dewhirst. "Fourier analysis of fluctuations of oxygen tension and blood flow in R3230Ac tumors and muscle in rats." American Journal of Physiology-Heart and Circulatory Physiology 277, no. 2 (August 1, 1999): H551—H568. http://dx.doi.org/10.1152/ajpheart.1999.277.2.h551.
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Tumor hypoxia is a major barrier to tumor radiation therapy. Typically tumor hypoxia occurs in two forms: chronic and acute. Although the existence of acute hypoxia has long been acknowledged, its temporal characteristics have never been directly measured and documented. In this study tumor[Formula: see text], blood flow (BF), and arterial blood pressure (BP) were measured simultaneously in nine Fischer 344 rats bearing R3230Ac rat mammary adenocarcinomas in the subcutis of the left hindleg. We measured [Formula: see text] at a single location for 36–125 min using recessed-tip oxygen microelectrodes. Simultaneously, we measured tumor BF at two sites within the tumor using laser-Doppler flowmetry (LDF). Similar recordings were made in the quadriceps muscle of seven non-tumor-bearing rats. The [Formula: see text], tumor BF, and BP records were subjected to Fourier analysis.[Formula: see text] and BF showed low-frequency fluctuations (<2 cycles/min) in both tumor and muscle, but the magnitude of the changes in tumor was greater. Tumor BF showed more activity at low frequencies than muscle BF, and the magnitude tended to be greater. No strong correlations were found between[Formula: see text] and BF power spectra for either tumor or muscle or between the frequency patterns of BP and tumor[Formula: see text] spectra. These results quantitatively demonstrate, for the first time, that BF and[Formula: see text] fluctuate at very low frequencies in tumors. In addition to having biological significance for tumor therapy, these fluctuations may have the potential to alter tumor cell behavior via induction of hypoxia reoxygenation injury and/or altered gene expression.
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Granneman, J. G., M. Burnazi, Z. Zhu, and L. A. Schwamb. "White adipose tissue contributes to UCP1-independent thermogenesis." American Journal of Physiology-Endocrinology and Metabolism 285, no. 6 (December 2003): E1230—E1236. http://dx.doi.org/10.1152/ajpendo.00197.2003.
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β3-Adrenergic receptors (AR) are nearly exclusively expressed in brown and white adipose tissues, and chronic activation of these receptors by selective agonists has profound anti-diabetes and anti-obesity effects. This study examined metabolic responses to acute and chronic β3-AR activation in wild-type C57Bl/6 mice and congenic mice lacking functional uncoupling protein (UCP)1, the molecular effector of brown adipose tissue (BAT) thermogenesis. Acute activation of β3-AR doubled metabolic rate in wild-type mice and sharply elevated body temperature and BAT blood flow, as determined by laser Doppler flowmetry. In contrast, β3-AR activation did not increase BAT blood flow in mice lacking UCP1 (UCP1 KO). Nonetheless, β3-AR activation significantly increased metabolic rate and body temperature in UCP1 KO mice, demonstrating the presence of UCP1-independent thermogenesis. Daily treatment with the β3-AR agonist CL-316243 (CL) for 6 days increased basal and CL-induced thermogenesis compared with naive mice. This expansion of basal and CL-induced metabolic rate did not require UCP1 expression. Chronic CL treatment of UCP1 KO mice increased basal and CL-stimulated metabolic rate of epididymal white adipose tissue (EWAT) fourfold but did not alter BAT thermogenesis. After chronic CL treatment, CL-stimulated thermogenesis of EWAT equaled that of interscapular BAT per tissue mass. The elevation of EWAT metabolism was accompanied by mitochondrial biogenesis and the induction of genes involved in lipid oxidation. These observations indicate that chronic β3-AR activation induces metabolic adaptation in WAT that contributes to β3-AR-mediated thermogenesis. This adaptation involves lipid oxidation in situ and does not require UCP1 expression.
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Mansour, Ahmed, Sherif Rashad, Kuniyasu Niizuma, Miki Fujimura, and Teiji Tominaga. "A novel model of cerebral hyperperfusion with blood-brain barrier breakdown, white matter injury, and cognitive dysfunction." Journal of Neurosurgery 133, no. 5 (November 2020): 1460–72. http://dx.doi.org/10.3171/2019.7.jns19212.
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OBJECTIVECerebral hyperperfusion (CHP) is associated with considerable morbidity. Its pathophysiology involves disruption of the blood-brain barrier (BBB) with subsequent events such as vasogenic brain edema and ischemic and/or hemorrhagic complications. Researchers are trying to mimic the condition of CHP; however, a proper animal model is still lacking. In this paper the authors report a novel surgically induced CHP model that mimics the reported pathophysiology of clinical CHP including BBB breakdown, white matter (WM) injury, inflammation, and cognitive impairment.METHODSMale Sprague-Dawley rats were subjected to unilateral common carotid artery (CCA) occlusion and contralateral CCA stenosis. Three days after the initial surgery, the stenosis of CCA was released to induce CHP. Cortical regional cerebral blood flow was measured using laser speckle flowmetry. BBB breakdown was assessed by Evans blue dye extravasation and matrix metalloproteinase–9 levels. WM injury was investigated with Luxol fast blue staining. Cognitive function was assessed using the Barnes circular maze. Other changes pertaining to inflammation were also assessed. Sham-operated animals were prepared and used as controls.RESULTSCerebral blood flow was significantly raised in the cerebral cortex after CHP induction. CHP induced BBB breakdown evident by Evans blue dye extravasation, and matrix metalloproteinase–9 was identified as a possible culprit. WM degeneration was evident in the corpus callosum and corpus striatum. Immunohistochemistry revealed macrophage activation and glial cell upregulation as an inflammatory response to CHP in the striatum and cerebral cortex. CHP also caused significant impairments in spatial learning and memory compared with the sham-operated animals.CONCLUSIONSThe authors report a novel CHP model in rats that represents the pathophysiology of CHP observed in various clinical scenarios. This model was produced without the use of pharmacological agents; therefore, it is ideal to study the pathology of CHP as well as to perform preclinical drug trials.
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Mansour, Ahmed, Kuniyasu Niizuma, Sherif Rashad, Akira Sumiyoshi, Rie Ryoke, Hidenori Endo, Toshiki Endo, Kenichi Sato, Ryuta Kawashima, and Teiji Tominaga. "A refined model of chronic cerebral hypoperfusion resulting in cognitive impairment and a low mortality rate in rats." Journal of Neurosurgery 131, no. 3 (September 2019): 892–902. http://dx.doi.org/10.3171/2018.3.jns172274.
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OBJECTIVEThe cognitive deficits of vascular dementia and the vasoocclusive state of moyamoya disease have often been mimicked with bilateral stenosis/occlusion of the common carotid artery (CCA) or internal carotid artery. However, the cerebral blood flow (CBF) declines abruptly in these models after ligation of the CCA, which differs from “chronic” cerebral hypoperfusion. While some modified but time-consuming techniques have used staged occlusion of both CCAs, others used microcoils for CCA stenosis, producing an adverse effect on the arterial endothelium. Thus, the authors developed a new chronic cerebral hypoperfusion (CCH) model with cognitive impairment and a low mortality rate in rats.METHODSMale Sprague-Dawley rats were subjected to unilateral CCA occlusion and contralateral induction of CCA stenosis (modified CCA occlusion [mCCAO]) or a sham operation. Cortical regional CBF (rCBF) was measured using laser speckle flowmetry. Cognitive function was assessed using a Barnes circular maze (BCM). MRI studies were performed 4 weeks after the operation to evaluate cervical and intracranial arteries and parenchymal injury. Behavioral and histological studies were performed at 4 and 8 weeks after surgery.RESULTSThe mCCAO group revealed a gradual CBF reduction with a low mortality rate (2.3%). White matter degeneration was evident in the corpus callosum and corpus striatum. Although the cellular density declined in the hippocampus, MRI revealed no cerebral infarctions after mCCAO. Immunohistochemistry revealed upregulated inflammatory cells and angiogenesis in the hippocampus and cerebral cortex. Results of the BCM assessment indicated significant impairment in spatial learning and memory in the mCCAO group. Although some resolution of white matter injury was observed at 8 weeks, the animals still had cognitive impairment.CONCLUSIONSThe mCCAO is a straightforward method of producing a CCH model in rats. It is associated with a low mortality rate and could potentially be used to investigate vascular disease, moyamoya disease, and CCH. This model was verified for an extended time point of 8 weeks after surgery.
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Wolf, Tilo, Ute Lindauer, Uwe Reuter, Tobias Back, Arno Villringer, Karl Einhäupl, and Ulrich Dirnagl. "Noninvasive near Infrared Spectroscopy Monitoring of Regional Cerebral Blood Oxygenation Changes during Peri-Infarct Depolarizations in Focal Cerebral Ischemia in the Rat." Journal of Cerebral Blood Flow & Metabolism 17, no. 9 (September 1997): 950–54. http://dx.doi.org/10.1097/00004647-199709000-00004.
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Intermittent peri-infarct depolarizations (PID), which spread from the vicinity of the infarction over the cortex, have been reported in focal ischemia. These depolarizations resemble cortical spreading depression except that they damage the cortex and enlarge the infarct volume possibly because of compromised oxygen delivery. The main purpose of this study was to evaluate the noninvasive technique of near-infrared spectroscopy (NIRS) for the identification of PID and to evaluate its capability for further pathophysiological studies. We used male barbiturate-anesthetized Wistar rats (n = 10) in which middle cerebral artery occlusion had been performed with a surgical thread. Middle cerebral artery occlusion resulted in a drop in parietally measured regional cerebral blood flow (laser Doppler flowmetry) to 31 ± 8% of baseline flow. Six ± 4 minutes after the induction of focal ischemia, 5 ± 2 direct current deflections were recorded during a one-hour measurement period which may be regarded as PID. Measuring regional cerebral blood oxygenation changes with a NIRO 500 revealed dynamic concentration changes in the three chromophores oxyhemoglobin [HbO2], deoxyhemoglobin [Hb], and the oxidized form of cytochrome aa3 [CytO] during PID. Typically, an initial slight decrease of [HbO2] (−6.1 ± 1.7 arbitrary units [AU]) and an increase of [Hb] (+1 1.5 ± 7.7 AU) were followed by an increase of [HbO2] (+10.8 ± 4.7 AU) and a decrease of [Hb] (−4.7 ± 5.5 AU); [CytO] decreased during the depolarizations (−2.0 ± 1.2 AU). We conclude that NIRS can detect typical PID-associated changes in blood oxygenation. We hypothesize that during the course of PID, unlike “normal” spreading depression, hypoxygenation precedes hyperoxygenation of the microcirculation in a given cortex volume as the depolarization wave propagates through hemodynamically compromised to intact tissue. This would accord with the known damaging effect of PID. The NIRS “fingerprint” of PID encourages the search for PID during early stroke in patients.
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Chauhan, Anil, Mohammad M. Khan, Chintan Gandhi, Neelam Chauhan, Asgar Zaheer, David G. Motto, and Steven R. Lentz. "EDA-Containing Fibronectin Aggravates Ischemic Brain Injury In Mice." Blood 116, no. 21 (November 19, 2010): 330. http://dx.doi.org/10.1182/blood.v116.21.330.330.
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Abstract Abstract 330 Background: Fibronectin (FN) is a dimeric glycoprotein that plays an important role in several cellular processes, such as embryogenesis, malignancy, hemostasis, wound healing and maintenance of tissue integrity. FN is a ligand for many members of the integrin family (e.g. αIIbβ3, α5β1, α4β1, α9β1, αvβ3 and αvβ5) and also binds to thrombosis-related proteins including heparin, collagen and fibrin. FN generates protein diversity as a consequence of alternative processing of a single primary transcript. Two forms of FN exist; soluble plasma FN (pFN), which lacks the alternatively-spliced Extra Domain A (EDA); and insoluble cellular FN (cFN), which contains EDA. FN containing EDA (EDA+FN) is normally absent in plasma of human and mouse but EDA+FN has been found in patients with vascular injury secondary to vasculitis, sepsis, acute major trauma or ischemic stroke. We tested the hypothesis that elevated levels of plasma EDA+FN increase brain injury in an experimental model of ischemic stroke in mice. Model and Method: We used two genetically modified mouse strains: EDA+/+ mice contain optimized spliced sites at both splicing junctions of the EDA exon and constitutively express only EDA+FN, whereas EDA-/- mice contain an EDA-null allele of the EDA exon and express only FN lacking EDA. Control EDAwt/wt mice contain the wild-type FN allele. Transient focal cerebral ischemia was induced by 60 minutes of occlusion of the right middle cerebral artery with a 7.0 siliconized filament in male mice (8-10 weeks in age). Mice were anesthetized with 1–1.5% isoflurane mixed with medical air. Body temperature was maintained at 37°C ± 1.0 using a heating pad. Laser Doppler flowmetry was used to confirm induction of ischemia and reperfusion. At 23 hours after MCAO, mice were evaluated for neurological deficits as a functional outcome and were sacrificed for quantification of infarct volume. For morphometric measurement eight 1 mm coronal sections were stained with 2% triphenyl-2, 3, 4-tetrazolium-chloride (TTC). Sections were digitalized and infarct areas were measured blindly using NIS elements. Result: In EDA+/+ mice the percentage of infarct volume (mean ± SEM: 37.25 ± 4.11, n= 12,) in the ipsilateral (ischemic) hemisphere was increased by approximately two-fold compared to EDA wt/wt mice (mean ± SEM: 22.33 ± 3.39, n=11; P< 0.05, ANOVA) or EDA-/- mice (mean ± SEM: 21.72 ± 2.94, n=9). Regional cerebral blood flow during ischemia was not different among groups as assessed by laser Doppler flowmetry. The percentage increase in infarct volume in the EDA+/+ mice correlated well with severe neurological deficits (motor-deficit assessed by a four-point neurological score scale) compared to EDA wt/wt or EDA-/- mice. Because both thrombosis and inflammation contributes to brain injury during ischemic stroke, we investigated the time to form an occlusive thrombus in ferric-chloride carotid artery injury model by intravital microscopy. EDA+/+ mice demonstrated significantly faster time to occlusion (mean ± SEM: 12.35 ± 1.51 n=12,) compared to EDAwt/wt (Mean ± SEM: 17.27 ± 1.72 min, n=13, P<0.05, ANOVA) or EDA-/- (Mean ± SEM: 15.61 ± 1.76, n=11) mice. Additionally, the inflammatory response in the ischemic region was increased by two fold in EDA+/+ mice compared to EDA wt/wt and EDA-/- mice as sensed by myeloperoxidase activity and immunohistochemical analysis of neutrophils. Conclusion: EDA-containing FN is pro-thrombotic and pro-inflammatory, and aggravates ischemic brain injury in an experimental model of stroke in mice. The presence of EDA+FN in plasma may be a risk factor for vascular injury secondary to ischemic stroke. Disclosures: No relevant conflicts of interest to declare.
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Lee, Jin-Yul, Dah-Luen Huang, Richard Keep, and Oren Sagher. "Effect of electrical stimulation of the cervical spinal cord on blood flow following subarachnoid hemorrhage." Journal of Neurosurgery 109, no. 6 (December 2008): 1148–54. http://dx.doi.org/10.3171/jns.2008.109.12.1148.
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Object Cervical spinal cord stimulation (SCS) increases global cerebral blood flow (CBF) and ameliorates cerebral ischemia according to a number of experimental models as well as some anecdotal reports in humans. Nonetheless, such stimulation has not been systematically applied for use in cerebral vasospasm. In the present study the authors examined the effect of cervical SCS on cerebral vasoconstriction in a double-hemorrhage model in rats. Methods Subarachnoid hemorrhage (SAH) was induced with 2 blood injections through an indwelling catheter in the cisterna magna. Spinal cord stimulation was applied 90 minutes after induction of the second SAH (Day 0) or on Day 5 post-SAH. Measurements of the basilar artery (BA) diameter and cross-sectional area and regional CBF (using laser Doppler flowmetry and 14C-radiolabeled N-isopropyl-p-iodoamphetamine hydrochloride) were obtained and compared between SAH and sham-operated control rats that did not receive SCS. Results At Day 0 after SAH, there were slight nonsignificant decreases in BA diameter and cross-sectional area (89 ± 3% and 81 ± 4%, respectively, of that in controls) in no-SCS rats. At this time point, BA diameter and crosssectional area were slightly increased (116 ± 6% and 132 ± 9%, respectively, compared with controls, p < 0.001) in SCS-treated rats. On Day 5 after SAH, no-SCS rats had marked decreases in BA diameter and cross-sectional area (64 ± 3% and 39 ± 4%, respectively, compared with controls, p < 0.001) and corrugation of the vessel wall. These changes were reversed in rats that had received SCS (diameter, 110 ± 9% of controls; area, 106 ± 4% of controls; p < 0.001). Subarachnoid hemorrhage reduced CBF at Days 0 and 5 post-SAH, and SCS increased flows at both time points, particularly in regions supplied by the middle cerebral artery. Conclusions Data in this study showed that SCS can reverse BA constriction and improve global CBF in this SAH model. Spinal cord stimulation may represent a useful adjunct in the treatment of vasospasm.
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Pfister, H. W., U. Koedel, R. L. Haberl, U. Dirnagl, W. Feiden, G. Ruckdeschel, and K. M. Einhäupl. "Microvascular Changes during the Early Phase of Experimental Bacterial Meningitis." Journal of Cerebral Blood Flow & Metabolism 10, no. 6 (November 1990): 914–22. http://dx.doi.org/10.1038/jcbfm.1990.148.
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We investigated the temporal profile of the changes in regional CBF (rCBF) and intracranial pressure (ICP) during the early phase of pneumococcal meningitis in the rat. rCBF, as measured by laser-Doppler flowmetry, and ICP were continuously monitored during 6 h post infection (p.i.). Brain edema formation was assessed by brain water content determinations. Meningitis was induced by intracisternal injection of 75 μl of 107 colony-forming units/ml pneumococci (n = 7). In control animals (n = 6), saline was injected. There was no change in the rCBF or ICP of controls throughout the experiment. However, there was a dramatic increase in rCBF and ICP associated with brain edema formation in untreated meningitis animals. rCBF increased to 135.3 ± 33.8% (mean ± SD) in the untreated animals at 1 h p.i, and reached 211.1 ± 40.5% at 6 h p.i. (p < 0.05 compared with controls). ICP increased from 2.9 ± 1.4 to 10.4 ± 4.7 mm Hg at 6 h p.i. (p < 0.05 compared with controls). Brain water content was significantly elevated (79.69 ± 0.24 compared with 78.94 ± 0.16% in the control group, p < 0.05). We investigated the effect of dexamethasone (3 mg/kg i.p.), which was given prior to the induction of meningitis (n = 3) or at 2 h after pneumococcal injection (n = 5), indomethacin (10 mg/kg i.V., n = 5), and superoxide dismutase (SOD; 132,000 U/kg i.v. per 6 h, n = 6). The increases in rCBF and ICP were prevented by the pretreatment with dexamethasone and the administration of SOD, delayed and attenuated by pretreatment with indomethacin, and reversed by administration of dexamethasone 2 h p.i. These findings suggest that oxygen-derived free radicals are involved as mediators in the increases of rCBF and ICP and brain edema formation during the early phase of experimental bacterial meningitis. Arachidonic acid metabolites of the cyclooxygenase pathway are partially involved in the observed changes and are one possible source for the generation of oxygen-derived free radicals in bacterial meningitis.
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Salvi, Paolo, Andrea Faini, Paolo Castiglioni, Fausto Brunacci, Luca Montaguti, Francesca Severi, Sylvie Gautier, Enzo Pretolani, Athanase Benetos, and Gianfranco Parati. "Increase in slow-wave vasomotion by hypoxia and ischemia in lowlanders and highlanders." Journal of Applied Physiology 125, no. 3 (September 1, 2018): 780–89. http://dx.doi.org/10.1152/japplphysiol.00977.2017.
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The physiological relevance of slow-wave vasomotion is still unclear, even though it has been hypothesized that it could be a compensatory mechanism for enhancing tissue oxygenation in conditions of reduced oxygen supply. The aim of our study was to explore the effects of hypoxia and ischemia on slow-wave vasomotion in microcirculation. Peripheral oxygen saturation and forearm microcirculation flow (laser-Doppler flowmetry) were recorded at baseline and during postocclusive reactive hyperemia in the Himalaya region from 8 European lowlanders (6 men; aged 29–39 yr) at 1,350, 3,400, and 5,050 m and from 10 Nepalese male highlanders (aged 21–39 yr) at 3,400 and 5,050 m of altitude. The same measurements were also performed at sea level in 16 healthy volunteers (aged 23–61 yr) during a short-term exposure to normobaric hypoxia. In lowlanders, exposure to progressively higher altitude under baseline flow conditions progressively increased 0.06–0.15 Hz vasomotion amplitude [power spectral density % was expressed as geometric means (geometric standard deviation) = 14.0 (3.6) at 1,350 m; 87.0(2.3) at 3,400 m and 249.8 (3.6) at 5,050 m; P = 0.006 and P < 0.001 vs. 1,350 m, respectively]. In highlanders, low frequency vasomotion amplitude was similarly enhanced at different altitudes [power spectral density % = 183.4 (4.1) at 3,400 m vs. 236.0 (3.0) at 5,050 m; P = 0.139]. In both groups at altitude, it was further increased after ischemic stimulus ( P < 0.001). At baseline, acute short lasting normobaric hypoxia did not induce low frequency vasomotion, which was conversely induced by ischemia, even under normal oxygenation and barometric pressure. This study offers the demonstration of a significant increase in slow-wave vasomotion under prolonged hypobaric-hypoxia exposure at high altitude, with a further enhancement after ischemia induction. NEW & NOTEWORTHY This study offers the demonstration in humans of the occurrence of enhanced slow-wave vasomotion in microcirculation induced by exposure to hypobaric hypoxia, ischemia, and their combination. This phenomenon, where vasomotion can be hypothesized to behave as a “peripheral heart,” may represent a compensating adaptive change aimed at improving peripheral flow and tissue oxygenation in conditions of reduced oxygen supply, such as altitude-induced hypobaric hypoxia and postocclusion ischemia.
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Denorme, Frederik, Bhanu Kanth Manne, Yasuhiro Kosaka, Benjamin Kile, Matthew T. Rondina, and Robert A. Campbell. "Cyclophilin D Mediated Platelet Necrosis Regulates Ischemic Stroke Outcomes in Mice." Blood 134, Supplement_1 (November 13, 2019): 3620. http://dx.doi.org/10.1182/blood-2019-123839.
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Background: Anti-platelet agents are used clinically to prevent ischemic stroke but are incompletely effective. Emerging evidence highlights that platelets contribute to ischemic stroke through mechanisms and pathways that are not targeted by classic anti-platelet agents. Besides their role in thrombosis, platelets also mediate inflammation through the formation of heterotypic leukocyte aggregates. In particular, platelet-neutrophil interactions are known to promote brain injury following ischemic stroke. However, the mechanism by which platelets interact with neutrophils and promote thromboinflammation in ischemic stroke remains elusive. Recently, cyclophilin D (CypD)-mediated platelet necrosis emerged as a potential mediator of detrimental platelet-neutrophil interactions. Aims: To investigate the role of CypD-mediated platelet necrosis in the setting of acute ischemic stroke. Methods: Mice harboring a floxed allele of CypD were crossed to animals expressing Cre recombinase controlled by the Pf4 promoter to generate platelet-specific CypD deficient mice (KO). KO mice and littermate controls (WT)were subjected to a transient middle cerebral artery occlusion (tMCAO) model with 1h of cerebral ischemia followed by 23h of reperfusion or a permanent MCAO model with 24h of ischemia. Neurological and motor outcomes and brain infarct size were measured 24h after stroke onset. In addition, we examined both circulating and cerebral platelet-neutrophil aggregates 24h after stroke. Cerebral blood flow was monitored via blood laser doppler flowmetry. Neutrophils were depleted 24h before stroke onset using a neutrophil-depleting antibody to examine the contribution of neutrophils in ischemic stroke. Results: Loss of CypD in platelets significantly improved neurological (p<0.001) and motor (p<0.005) functions and reduced ischemic stroke infarct volume (p<0.0001) after cerebral transient ischemia/reperfusion injury compared to WT controls. To determine whether improved stroke outcomes in KO mice was associated with improved local cerebral blood flow (CBF) during reperfusion, CBF was measured at time points during and after stroke induction. During ischemia, and immediately after reperfusion, CBF was similar in WTand KO mice. Nevertheless, 3h after stroke onset, CBF was significantly greater (48±15% vs 31±10%; p<0.05) in KO mice compared to WTmice. This difference in CBF persisted and was even more pronounced at 24h (54±12% vs 27±8%; p<0.01). To further investigate whether platelet necrosis was contributing to brain infarction during cerebral reperfusion, we employed a permanent MCAO model. With permanent occlusion, no differences were observed in infarct volume, neurological functions, or motor functions between WT or KO mice, suggesting platelet CypD specifically mediates reperfusion injury following transient cerebral ischemia. These detrimental effects of platelet necrosis were attributable, in part, to platelet-neutrophil interactions. Twenty-four hours after stroke, significantly (p<0.01) fewer circulating platelet-neutrophil aggregates were found in KO mice. Underscoring the role of platelet necrosis in this process, we observed that 33±4% of platelets in platelet-neutrophil aggregates expressed phosphatidylserine (PS) on their surface in WTmice. In contrast, only 17.8±5.1% of platelets in platelet-neutrophil aggregates were PS-positive in KO counterparts (p<0.01). Furthermore, KO mice had less neutrophils recruited to their brain relative to WT controls, and cerebral platelet-neutrophil aggregates were virtually absent in KO mice. To determine whether the protective effect observed in KOmice was due to reduced interactions between necrotic platelets and neutrophils, we depleted circulating neutrophils 24h before induction of stroke. Depletion of neutrophils significantly (p<0.05) reduced infarct size and neurological damage following ischemic stroke in WTmice. However, neutrophil depletion conferred no additional protective effect in KOanimals. Conclusions: These results suggest necrotic platelets interact with neutrophils to exacerbate brain injury following ischemic stroke. As inhibiting platelet necrosis does not compromise hemostasis, targeting platelet CypD may be a potential therapeutic strategy to limit brain damage following ischemic stroke. Disclosures No relevant conflicts of interest to declare.
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Drexler, P., P. Fiala, R. Kadlec, P. Londak, T. Madrova, M. Klima, and J. Zukal. "Numerical modeling and experimental verification of a low fluid flow inductive flowmeter." Flow Measurement and Instrumentation, January 2021, 101876. http://dx.doi.org/10.1016/j.flowmeasinst.2020.101876.
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"On the Issue of Development of Propeller Flowmeters Design all over the World." Water sector of Russia: problems, technologies, management, no. 1, 2011 (2011): 82–102. http://dx.doi.org/10.35567/1999-4508-2011-1-7.
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A propeller flowmeter is the most developed and wide-spread instrument for measurement of flow velocity in rivers and canals all over the world (in spite of the active development over the recent years of instruments based upon M. Faraday induction currents or C. Doppler effect). This instrument history is more than two centuries long. The paper dwells on the main trends of the hydrometric instrument-building industry development all over the world, as well as history of appearance and development of the device in terms of its main components optimization. Analysis and comparison of currently produced propeller flowmeters have been carried out.
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"Committee Report: Magnetic Inductive Flowmeters." Journal - American Water Works Association 99, no. 6 (June 2007): 154–60. http://dx.doi.org/10.1002/j.1551-8833.2007.tb07963.x.
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"Modelling of induction rotary permanent magnet flowmeters for liquid metal flow control." Magnetohydrodynamics 50, no. 2 (June 2014): 157–64. http://dx.doi.org/10.22364/mhd.50.2.4.
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