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Journal articles on the topic 'Cerebral Arteriole'
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1
Baker, Wesley B., Ashwin B. Parthasarathy, Kimberly P. Gannon, Venkaiah C. Kavuri, David R. Busch, Kenneth Abramson, Lian He, et al. "Noninvasive optical monitoring of critical closing pressure and arteriole compliance in human subjects." Journal of Cerebral Blood Flow & Metabolism 37, no. 8 (May 25, 2017): 2691–705. http://dx.doi.org/10.1177/0271678x17709166.
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The critical closing pressure ( CrCP) of the cerebral circulation depends on both tissue intracranial pressure and vasomotor tone. CrCP defines the arterial blood pressure ( ABP) at which cerebral blood flow approaches zero, and their difference ( ABP − CrCP) is an accurate estimate of cerebral perfusion pressure. Here we demonstrate a novel non-invasive technique for continuous monitoring of CrCP at the bedside. The methodology combines optical diffuse correlation spectroscopy (DCS) measurements of pulsatile cerebral blood flow in arterioles with concurrent ABP data during the cardiac cycle. Together, the two waveforms permit calculation of CrCP via the two-compartment Windkessel model for flow in the cerebral arterioles. Measurements of CrCP by optics (DCS) and transcranial Doppler ultrasound (TCD) were carried out in 18 healthy adults; they demonstrated good agreement (R = 0.66, slope = 1.14 ± 0.23) with means of 11.1 ± 5.0 and 13.0 ± 7.5 mmHg, respectively. Additionally, a potentially useful and rarely measured arteriole compliance parameter was derived from the phase difference between ABP and DCS arteriole blood flow waveforms. The measurements provide evidence that DCS signals originate predominantly from arteriole blood flow and are well suited for long-term continuous monitoring of CrCP and assessment of arteriole compliance in the clinic.
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Xi, Qi, Edward Umstot, Guiling Zhao, Damodaran Narayanan, Charles W. Leffler, and Jonathan H. Jaggar. "Glutamate regulates Ca2+ signals in smooth muscle cells of newborn piglet brain slice arterioles through astrocyte- and heme oxygenase-dependent mechanisms." American Journal of Physiology-Heart and Circulatory Physiology 298, no. 2 (February 2010): H562—H569. http://dx.doi.org/10.1152/ajpheart.00823.2009.
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Glutamate is the principal cerebral excitatory neurotransmitter and dilates cerebral arterioles to match blood flow to neural activity. Arterial contractility is regulated by local and global Ca2+ signals that occur in smooth muscle cells, but modulation of these signals by glutamate is poorly understood. Here, using high-speed confocal imaging, we measured the Ca2+ signals that occur in arteriole smooth muscle cells of newborn piglet tangential brain slices, studied signal regulation by glutamate, and investigated the physiological function of heme oxygenase (HO) and carbon monoxide (CO) in these responses. Glutamate elevated Ca2+ spark frequency by ∼188% and reduced global intracellular Ca2+ concentration ([Ca2+]i) to ∼76% of control but did not alter Ca2+ wave frequency in brain arteriole smooth muscle cells. Isolation of cerebral arterioles from brain slices abolished glutamate-induced Ca2+ signal modulation. In slices treated with l-2-α-aminoadipic acid, a glial toxin, glutamate did not alter Ca2+ sparks or global [Ca2+]i but did activate Ca2+ waves. This shift in Ca2+ signal modulation by glutamate did not occur in slices treated with d-2-α-aminoadipic acid, an inactive isomer of l-2-α-aminoadipic acid. In the presence of chromium mesoporphyrin, a HO blocker, glutamate inhibited Ca2+ sparks and Ca2+ waves and did not alter global [Ca2+]i. In isolated arterioles, CORM-3 [tricarbonylchloro(glycinato)ruthenium(II)], a CO donor, activated Ca2+ sparks and reduced global [Ca2+]i. These effects were blocked by 1 H-(1,2,4)-oxadiazolo-(4,3-a)-quinoxalin-1-one, a soluble guanylyl cyclase inhibitor. Collectively, these data indicate that glutamate can modulate Ca2+ sparks, Ca2+ waves, and global [Ca2+]i in arteriole smooth muscle cells via mechanisms that require astrocytes and HO. These data also indicate that soluble guanylyl cyclase is involved in CO activation of Ca2+ sparks in arteriole smooth muscle cells.
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Liang, Guo Hua, Adebowale Adebiyi, M. Dennis Leo, Elizabeth M. McNally, Charles W. Leffler, and Jonathan H. Jaggar. "Hydrogen sulfide dilates cerebral arterioles by activating smooth muscle cell plasma membrane KATP channels." American Journal of Physiology-Heart and Circulatory Physiology 300, no. 6 (June 2011): H2088—H2095. http://dx.doi.org/10.1152/ajpheart.01290.2010.
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Hydrogen sulfide (H2S) is a gaseous signaling molecule that appears to contribute to the regulation of vascular tone and blood pressure. Multiple potential mechanisms of vascular regulation by H2S exist. Here, we tested the hypothesis that piglet cerebral arteriole smooth muscle cells generate ATP-sensitive K+ (KATP) currents and that H2S induces vasodilation by activating KATP currents. Gas chromatography/mass spectrometry data demonstrated that after placing Na2S, an H2S donor, in solution, it rapidly (1 min) converts to H2S. Patch-clamp electrophysiology indicated that pinacidil (a KATP channel activator), Na2S, and NaHS (another H2S donor) activated K+ currents at physiological steady-state voltage (−50 mV) in isolated cerebral arteriole smooth muscle cells. Glibenclamide, a selective KATP channel inhibitor, fully reversed pinacidil-induced K+ currents and partially reversed (∼58%) H2S-induced K+ currents. Western blot analysis indicated that piglet arterioles expressed inwardly rectifying K+ 6.1 (Kir6.1) channel and sulfonylurea receptor 2B (SUR2B) KATP channel subunits. Pinacidil dilated pressurized (40 mmHg) piglet arterioles, and glibenclamide fully reversed this effect. Na2S also induced reversible and repeatable vasodilation with an EC50 of ∼30 μM, and this effect was partially reversed (∼55%) by glibenclamide. Vasoregulation by H2S was also studied in pressurized resistance-size cerebral arteries of mice with a genetic deletion in the gene encoding SUR2 (SUR2 null). Pinacidil- and H2S-induced vasodilations were smaller in arterioles of SUR2 null mice than in wild-type controls. These data indicate that smooth muscle cell KATP currents control newborn cerebral arteriole contractility and that H2S dilates cerebral arterioles by activating smooth muscle cell KATP channels containing SUR2 subunits.
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Wu, Xu-Dong, Chen Wang, Zhen-Ying Zhang, Yan Fu, Feng-Ying Liu, and Xiu-Hua Liu. "PuerarinAttenuates Cerebral Damage by Improving Cerebral Microcirculation in Spontaneously Hypertensive Rats." Evidence-Based Complementary and Alternative Medicine 2014 (2014): 1–7. http://dx.doi.org/10.1155/2014/408501.
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Puerariae Lobatae Radix(Gegen in Chinese) is the dried root ofPueraria lobata, a semiwoody, perennial, and leguminous vine native to China.Puerarinis one of the effective components of isoflavones isolated from the root ofPueraria lobata. Previous studies showed that extracts derived from the root ofPueraria lobatapossessed antihypertensive effect. Our study is to investigate whetherpuerarincontributes to prevention of stroke by improving cerebral microcirculation in rats.Materials and Methods. Video microscopy and laser Doppler perfusion imaging on the pia mater were used to measure the diameter of microvessel and blood perfusion in 12-week old spontaneously hypertensive rats (SHRs) and age-matched normotensive WKY rats. Histological alterations were observed by hematoxylin and eosin staining, and microvessel density in cerebral tissue was measured by immunohistochemical analysis with anti-Factor VIII antibody. Cell proliferation was detected by [3H]-TdR incorporation, and activities of p42/44 mitogen activated protein kinases (p42/44 MAPKs) were detected by western blot analysis in cultured cerebral microvascular endothelial cells (MECs).Results. Intravenous injection ofpuerarinrelaxed arterioles and increased the blood flow perfusion in the pia mater in SHRs.Puerarintreatment for 14 days reduced the blood pressure to a normal level in SHRs (P<0.05) and increased the arteriole diameter in the pia mater significantly as compared with vehicle treatment. Arteriole remodeling, edema, and ischemia in cerebral tissue were attenuated inpuerarin-treated SHRs. Microvessel density in cerebral tissue was greater withpuerarinthan with vehicle treatment.Puerarin-treated MECs showed greater proliferation and p42/44 MAPKs activities than vehicle treatment.Conclusions.Puerarinpossesses effects of antihypertension and stroke prevention by improved microcirculation in SHRs, which results from the increase in cerebral blood perfusion both by arteriole relaxation and p42/44 MAPKs-mediated angiogenesis.
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Beard, Daniel J., Damian D. McLeod, Caitlin L. Logan, Lucy A. Murtha, Mohammad S. Imtiaz, Dirk F. van Helden, and Neil J. Spratt. "Intracranial Pressure Elevation Reduces Flow through Collateral Vessels and the Penetrating Arterioles they Supply. a Possible Explanation for ‘Collateral Failure’ and Infarct Expansion after Ischemic Stroke." Journal of Cerebral Blood Flow & Metabolism 35, no. 5 (February 11, 2015): 861–72. http://dx.doi.org/10.1038/jcbfm.2015.2.
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Recent human imaging studies indicate that reduced blood flow through pial collateral vessels (‘collateral failure’) is associated with late infarct expansion despite stable arterial occlusion. The cause for ‘collateral failure’ is unknown. We recently showed that intracranial pressure (ICP) rises dramatically but transiently 24 hours after even minor experimental stroke. We hypothesized that ICP elevation would reduce collateral blood flow. First, we investigated the regulation of flow through collateral vessels and the penetrating arterioles arising from them during stroke reperfusion. Wistar rats were subjected to intraluminal middle cerebral artery (MCA) occlusion (MCAo). Individual pial collateral and associated penetrating arteriole blood flow was quantified using fluorescent microspheres. Baseline bidirectional flow changed to MCA-directed flow and increased by 4450% immediately after MCAo. Collateral diameter changed minimally. Second, we determined the effect of ICP elevation on collateral and watershed penetrating arteriole flow. Intracranial pressure was artificially raised in stepwise increments during MCAo. The ICP increase was strongly correlated with collateral and penetrating arteriole flow reductions. Changes in collateral flow post-stroke appear to be primarily driven by the pressure drop across the collateral vessel, not vessel diameter. The ICP elevation reduces cerebral perfusion pressure and collateral flow, and is the possible explanation for ‘collateral failure’ in stroke-in-progression.
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Ganjoo, Pragati, Neil E. Farber, Antal Hudetz, Jeremy J. Smith, Enric Samso, John P. Kampine, and William T. Schmeling. "In Vivo Effects of Dexmedetomidine on Laser-Doppler Flow and Pial Arteriolar Diameter." Anesthesiology 88, no. 2 (February 1, 1998): 429–39. http://dx.doi.org/10.1097/00000542-199802000-00022.
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Background The alpha2-adrenergic agonist dexmedetomidine alters global cerebral blood flow (CBF). However, few studies have investigated the action of dexmedetomidine on the cerebral microcirculation. This investigation examined the effects of dexmedetomidine on (1) regional CBF in the rat cerebral cortex using laser-Doppler flowmetry and (2) on pial arteriolar diameter. Methods Halothane-anesthetized rats were fitted with instruments to measure CBF as determined by laser-Doppler flow (CBFldf) or to measure pial arteriolar diameter by preparing a cranial hollow deepened until a translucent plate of skull remained, thereby maintaining the integrity of the cranial vault. In both groups, 20 microg/kg dexmedetomidine was infused intravenously. Thirty minutes later, the mean arterial pressure was restored to control values with an infusion of phenylephrine (0.5 to 5 microg/kg/min). Results Administration of dexmedetomidine was associated with decreases in end-tidal and arterial carbon dioxide. The CBFldf and pial arteriolar diameter were measured during normocapnia (controlled carbon dioxide) and during dexmedetomidine-induced hypocapnia. Intravenous administration of dexmedetomidine significantly decreased systemic arterial pressure concurrent with a decrease in CBFldf (22% in normocapnic animals, 36% in hypocapnic animals). Restoration of mean arterial pressure increased CBFldf in normocapnic but not in hypocapnic animals. Similarly, dexmedetomidine significantly reduced pial vessel diameter in both normocapnic (9%) and hypocapnic animals (17%). However, vessel diameters remained decreased in the normocapnic and hypocapnic animals after the mean arterial pressure was restored. Conclusions These results suggest a modulation of cerebral vascular autoregulation by dexmedetomidine which may be mediated, in part, by alterations in carbon dioxide. Dexmedetomidine may have a direct action on the cerebral vessels to reduce the CBF during normo- or hypocapnia. The differences between CBFldf and pial arteriole responses to restoration of mean arterial pressure may reflect the difference in measurement techniques because laser-Doppler measurements reflect the net effect of several arterial segments on microvascular perfusion, whereas diameter measurements specifically examined individual pial arterioles, suggesting that dexmedetomidine vasoconstriction in the cerebral vasculature may be differentially and regionally mediated.
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Iddings, Jennifer A., Ki Jung Kim, Yiqiang Zhou, Haruki Higashimori, and Jessica A. Filosa. "Enhanced Parenchymal Arteriole Tone and Astrocyte Signaling Protect Neurovascular Coupling Mediated Parenchymal Arteriole Vasodilation in the Spontaneously Hypertensive Rat." Journal of Cerebral Blood Flow & Metabolism 35, no. 7 (March 11, 2015): 1127–36. http://dx.doi.org/10.1038/jcbfm.2015.31.
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Functional hyperemia is the regional increase in cerebral blood flow upon increases in neuronal activity which ensures that the metabolic demands of the neurons are met. Hypertension is known to impair the hyperemic response; however, the neurovascular coupling mechanisms by which this cerebrovascular dysfunction occurs have yet to be fully elucidated. To determine whether altered cortical parenchymal arteriole function or astrocyte signaling contribute to blunted neurovascular coupling in hypertension, we measured parenchymal arteriole reactivity and vascular smooth muscle cell Ca2+ dynamics in cortical brain slices from normotensive Wistar Kyoto (WKY) and spontaneously hypertensive (SHR) rats. We found that vasoconstriction in response to the thromboxane A2 receptor agonist U46619 and basal vascular smooth muscle cell Ca2+ oscillation frequency were significantly increased in parenchymal arterioles from SHR. In perfused and pressurized parenchymal arterioles, myogenic tone was significantly increased in SHR. Although K+-induced parenchymal arteriole dilations were similar in WKY and SHR, metabotropic glutamate receptor activation-induced parenchymal arteriole dilations were enhanced in SHR. Further, neuronal stimulation-evoked parenchymal arteriole dilations were similar in SHR and WKY. Our data indicate that neurovascular coupling is not impaired in SHR, at least at the level of the parenchymal arterioles.
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Qi, Yujia, and Marcus Roper. "Control of low flow regions in the cortical vasculature determines optimal arterio-venous ratios." Proceedings of the National Academy of Sciences 118, no. 34 (August 19, 2021): e2021840118. http://dx.doi.org/10.1073/pnas.2021840118.
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The energy demands of neurons are met by a constant supply of glucose and oxygen via the cerebral vasculature. The cerebral cortex is perfused by dense, parallel arterioles and venules, consistently in imbalanced ratios. Whether and how arteriole–venule arrangement and ratio affect the efficiency of energy delivery to the cortex has remained an unanswered question. Here, we show by mathematical modeling and analysis of the mapped mouse sensory cortex that the perfusive efficiency of the network is predicted to be limited by low-flow regions produced between pairs of arterioles or pairs of venules. Increasing either arteriole or venule density decreases the size of these low-flow regions, but increases their number, setting an optimal ratio between arterioles and venules that matches closely that observed across mammalian cortical vasculature. Low-flow regions are reshaped in complex ways by changes in vascular conductance, creating geometric challenges for matching cortical perfusion with neuronal activity.
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Asano, Y., R. C. Koehler, T. Kawaguchi, and R. W. McPherson. "Pial arteriolar constriction to alpha 2-adrenergic agonist dexmedetomidine in the rat." American Journal of Physiology-Heart and Circulatory Physiology 272, no. 6 (June 1, 1997): H2547—H2556. http://dx.doi.org/10.1152/ajpheart.1997.272.6.h2547.
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Dexmedetomidine (Dex) is an alpha 2-adrenergic agonist that decreases cerebral blood flow (CBF) when administered systemically. It is unclear whether cerebral vasoconstriction is mediated by a local effect on cerebral vessels or by a remote neural mechanism. In the present study, we compared the pial arteriole responses to locally and systemically administered Dex with and without local application of the specific alpha 2-adrenergic antagonist atipamezole. Six groups of male rats (n = 7 each) were anesthetized with isoflurane and prepared for measurements of small (20-39 microns), medium (40-59 microns), and large (60-79 microns) pial arteriole diameter by intravital microscopy or for regional CBF measurement by the radiolabeled-microsphere method. Local application of Dex caused dose-dependent constriction that was significant starting at 10(-8) M for small and medium-sized arterioles and at 10(-7) M for large arterioles. Constriction to 10(-5) M in small [21 +/- 2% (SE)], medium (21 +/- 2%), and large (15 +/- 1%) arterioles was almost completely blocked by local application of 10(-4) M atipamezole. Intravenous administration of Dex at 1 microgram/kg decreased CBF and caused modest arteriolar constriction that began to resolve 8 min after administration. A dose of 10 micrograms/kg constricted arterioles of all sizes with constriction beginning to resolve after approximately 10 min. Local application of atipamezole (10(-4) M) slightly blunted the response to 1 micrograms/kg of intravenous Dex but did not substantially limit constriction after 10 micrograms/kg. These data demonstrate that pial arterioles are capable of substantial constriction to Dex by a local alpha 2-adrenergic mechanism. However, the inability of locally applied atipamezole to substantially inhibit the vasoconstrictor response to systemically administered Dex suggests that Dex might also cause vasoconstriction indirectly through actions at other sites in the central nervous system.
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Iliff, Jeffrey J., Raimondo D'Ambrosio, Al C. Ngai, and H. Richard Winn. "Adenosine receptors mediate glutamate-evoked arteriolar dilation in the rat cerebral cortex." American Journal of Physiology-Heart and Circulatory Physiology 284, no. 5 (May 1, 2003): H1631—H1637. http://dx.doi.org/10.1152/ajpheart.00909.2002.
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We tested the hypothesis that adenosine (Ado) mediates glutamate-induced vasodilation in the cerebral cortex by monitoring pial arteriole diameter in chloralose-anesthetized rats equipped with closed cranial windows. Topical application of 100 μM glutamate and 100 μM N-methyl-d-aspartate (NMDA) dilated pial arterioles (baseline diameter 25 ± 2 μm) by 17 ± 1% and 18 ± 4%, respectively. Coapplication of the nonselective Ado receptor antagonist theophylline (Theo; 10 μM) significantly reduced glutamate- and NMDA-induced vasodilation to 4 ± 2% ( P < 0.01) and 6 ± 2% ( P < 0.05), whereas the Ado A1 receptor antagonist 8-cyclopentyl-1,3-dipropylxanthine (0.1 μM) had no effect. Moreover, application of the Ado A2A receptor-selective antagonist 4-{2-[7-amino-2-(2-furyl)(1,2,4)triazolo(2,3-a)(1,3,5)triazin-5-ylamino]ethyl}phenol (ZM-241385), either by superfusion (0.1 μM, 1 μM) or intravenously (1 mg/kg), significantly inhibited the pial arteriole dilation response to glutamate. Neither Theo nor ZM-241385 affected vascular reactivity to mild hypercapnia induced by 5% CO2 inhalation. These results suggest that Ado contributes to the dilation of rat cerebral arterioles induced by exogenous glutamate, and that the Ado A2A receptor subtype may be involved in this dilation response.
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Chen, Xuming, Yuanyuan Jiang, Sangcheon Choi, Rolf Pohmann, Klaus Scheffler, David Kleinfeld, and Xin Yu. "Assessment of single-vessel cerebral blood velocity by phase contrast fMRI." PLOS Biology 19, no. 9 (September 9, 2021): e3000923. http://dx.doi.org/10.1371/journal.pbio.3000923.
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Current approaches to high-field functional MRI (fMRI) provide 2 means to map hemodynamics at the level of single vessels in the brain. One is through changes in deoxyhemoglobin in venules, i.e., blood oxygenation level–dependent (BOLD) fMRI, while the second is through changes in arteriole diameter, i.e., cerebral blood volume (CBV) fMRI. Here, we introduce cerebral blood flow–related velocity-based fMRI, denoted CBFv-fMRI, which uses high-resolution phase contrast (PC) MRI to form velocity measurements of flow. We use CBFv-fMRI in measure changes in blood velocity in single penetrating microvessels across rat parietal cortex. In contrast to the venule-dominated BOLD and arteriole-dominated CBV fMRI signals, CBFv-fMRI is comparable from both arterioles and venules. A single fMRI platform is used to map changes in blood pO2 (BOLD), volume (CBV), and velocity (CBFv). This combined high-resolution single-vessel fMRI mapping scheme enables vessel-specific hemodynamic mapping in animal models of normal and diseased states and further has translational potential to map vascular dementia in diseased or injured human brains with ultra–high-field fMRI.
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Shih, Andy Y., Beth Friedman, Patrick K. Drew, Philbert S. Tsai, Patrick D. Lyden, and David Kleinfeld. "Active Dilation of Penetrating Arterioles Restores Red Blood Cell Flux to Penumbral Neocortex after Focal Stroke." Journal of Cerebral Blood Flow & Metabolism 29, no. 4 (January 28, 2009): 738–51. http://dx.doi.org/10.1038/jcbfm.2008.166.
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Pial arterioles actively change diameter to regulate blood flow to the cortex. However, it is unclear whether arteriole reactivity and its homeostatic role of conserving red blood cell (RBC) flux remains intact after a transient period of ischemia. To examine this issue, we measured vasodynamics in pial arteriole networks that overlie the stroke penumbra during transient middle cerebral artery occlusion in rat. In vivo two-photon laser-scanning microscopy was used to obtain direct and repeated measurements of RBC velocity and lumen diameter of individual arterioles, from which the flux of RBCs was calculated. We observed that occlusion altered surface arteriole flow patterns in a manner that ensured undisrupted flow to penetrating arterioles throughout the imaging field. Small-diameter arterioles (< 23 µm), which included 88% of all penetrating arterioles, exhibited robust vasodilation over a 90-min occlusion period. Critically, persistent vasodilation compensated for an incomplete recovery of RBC velocity during reperfusion to enable a complete restoration of postischemic RBC flux. Further, histologic examination of tissue hypoxia suggested re-oxygenation through all cortical layers of the penumbra. These findings indicate that selective reactivity of small pial arterioles is preserved in the stroke penumbra and acts to conserve RBC flux during reperfusion.
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Touzani, Omar, Samuel Galbraith, Peter Siegl, and James McCulloch. "Endothelin-B Receptors in Cerebral Resistance Arterioles and their Functional Significance after Focal Cerebral Ischemia in Cats." Journal of Cerebral Blood Flow & Metabolism 17, no. 11 (November 1997): 1157–65. http://dx.doi.org/10.1097/00004647-199711000-00004.
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In the cerebral circulation, endothelin-A receptor activation mediates marked prolonged vasoconstriction whereas endothelin-B (ETB) receptor activation effects dilation. In contrast to some peripheral vascular beds, ETB receptor–induced vasoconstriction has not yet been demonstrated in brain vessels. In this study in chloralose-anesthetized cats, with perivascular microapplications of ETB selective agonist (BQ-3020) and antagonist (BQ-788), we investigated whether ETB receptor–mediated constriction could be uncovered in cortical arterioles in vivo. In addition, we examined whether normal dilator response to ETB receptor activation is preserved in postishemic cerebral arterioles. The first microapplication of the selective ETB receptor agonist BQ-3020 (1 μmol/L) onto a pial cortical arteriole elicited marked dilation (caliber increased by 26.3 ± 15.1% from preinjection baseline). A second application of BQ-3020 (10-minute interval) onto the same vessel failed to evoke any significant vasomotor response. Subsequent (third and fourth) adventitial microapplication of the ETB receptor agonist on the same arteriolar site effected a significant constriction of cerebral arterioles (−15.3 ± 12.7% and −9.7 ± 6.3% from preinjection baseline, respectively, at 20 and 30 minutes after the first application). The pial arterioles did not display tachyphylaxis to repeated applications of potassium (10 mmol/L). The perivascular application of the ETB receptor antagonist BQ-788 (0.001 to 1 μmol/L) had no effect on arteriolar caliber per se but blocked both BQ-3020–induced dilation (inhibitory concentration ∼ 5 nmol/L) and vasoconstriction elicited by repeated activation of ETB receptors. After middle cerebral artery occlusion, most of the arterioles examined displayed a sustained dilation. The microapplication of BQ-3020 into the perivascular space surrounding postischemic dilated arterioles elicited a constriction of a similar magnitude to that induced by application of CSF (−17 ± 7% and −17 ± 7% from preinjection baseline, respectively). The adventitial microapplication of the ETB receptor antagonist (BQ-788, 0.1 μmol/L) on postocclusion dilated pial arterioles effected no change in the arteriolar caliber when compared with preinjection baseline. This BQ-788–induced response was significantly different from that induced by perivascular microinjection of CSF ( P < 0.001, analysis of variance). These investigations indicate that (1) repeated activation of ETB receptors displays tachyphylaxis of the vasodilator response but also uncovers significant constriction of cerebral arterioles in vivo; (2) the ability of BQ-3020 to elicit dilation is lost within 30 minutes of induced focal ischemia; and (3) ETB-mediated contractile tone contributes in a small but significant manner in limiting postischemia dilation of cortical pial arterioles.
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Dagro, Amy M., and K. T. Ramesh. "A mechanism for injury through cerebral arteriole inflation." Biomechanics and Modeling in Mechanobiology 18, no. 3 (January 2, 2019): 651–63. http://dx.doi.org/10.1007/s10237-018-01107-z.
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Knecht, Kenneth R., Sarah Milam, Daniel A. Wilkinson, Alexander L. Fedinec, and Charles W. Leffler. "Time-dependent action of carbon monoxide on the newborn cerebrovascular circulation." American Journal of Physiology-Heart and Circulatory Physiology 299, no. 1 (July 2010): H70—H75. http://dx.doi.org/10.1152/ajpheart.00258.2010.
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Carbon monoxide (CO) causes cerebral arteriolar dilation in newborn pigs by the activation of large-conductance Ca2+-activated K+ channels. In adult rat cerebral and skeletal muscle arterioles, CO has been reported to produce constriction caused by the inhibition of nitric oxide (NO) synthase (NOS). We hypothesized that, in contrast to dilation to acute CO, more prolonged exposure of newborn cerebral arterioles to elevated CO produces constriction by reducing NO. In piglets with closed cranial windows, pial arteriolar responses to isoproterenol (10−6 M), sodium nitroprusside (SNP; 10−7 and 3 × 10−7 M), and l-arginine ethyl ester (l-Arg; 10−5 and 10−4 M) were determined before and after 2 h of treatment with CO. CO (10−7 M) caused transient dilation and had no further effects. CO (2 × 10−7 and 10−6 M) initially caused vasodilation, but over the 2-h exposure, pial arterioles constricted and removal of the CO caused dilation. Exposure to elevated CO (2 h) did not alter dilation to SNP or isoproterenol. Conversely, the NOS substrate l-Arg caused dilation before CO that was progressively lost over 90 min of elevated CO. If NO was held constant, CO caused dilation that was sustained for 2 h. We conclude that in neonates, cerebral arteriole responses to CO are biphasic: dilation to acute elevation with subsequent constriction from NOS inhibition after more prolonged exposure. As a result, short episodic production of CO allows function as a dilator gasotransmitter, whereas prolonged elevation can reduce NO to elevate cerebrovascular tone. The interaction between heme oxygenase/CO and NOS/NO could form a negative feedback system in the control of cerebral vascular tone.
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Saesue, Prajak, Tetsuyoshi Horiuchi, Tetsuya Goto, Yuichiro Tanaka, and Kazuhiro Hongo. "Functional role of the Na+/H+ exchanger in the regulation of cerebral arteriolar tone in rats." Journal of Neurosurgery 101, no. 2 (August 2004): 330–35. http://dx.doi.org/10.3171/jns.2004.101.2.0330.
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Object. In vascular smooth-muscle cells, the Na+/H+ exchanger (NHE) is involved in the regulation of [Na+]i, pHi through [H+], and cell volume. Recently, investigations have determined that this exchanger contributes to ischemia and reperfusion injury in coronary circulation. Nonetheless, there is limited information on this glycoprotein in cerebral circulation, especially microcirculation. Thus, the authors in the present study examined the role of NHE in the regulation of cerebral arteriolar tone and its related mechanisms in vitro. Methods. The internal diameter of isolated pressurized intracerebral arterioles in rats was monitored with the aid of a microscope. To examine the basal activity of NHE two kinds of Na+/H+ exchange inhibitors (FR183998 and 5-[N,N-hexamethylene] amiloride) were administered in the arterioles. Furthermore the authors studied the effects of nitric oxide (NO) synthase inhibitor (NG methyl-l-arginine), Na+/K+—adenosine triphosphatase (NKA) inhibitor (ouabain), and the Na+/Ca++ exchange inhibitor (SEA0400) on the vascular response induced by either of the Na+/H+ exchange inhibitors. Both of the Na+/H+ exchange inhibitors constricted the arteriole. Subsequent application of NO synthase inhibitor further decreased the diameter of the arterioles. The Na+/H+ exchange inhibitor—induced constriction was completely abolished in the presence of ouabain and SEA0400. Conclusions. The NHE is active in the basal condition and regulates cerebral arteriolar tone through NKA and the Na+/Ca++ exchanger. Endogenous NO is not related to the activity of NHE in basal conditions.
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Pinard, Elisabeth, Nicolas Engrand, and Jacques Seylaz. "Dynamic Cerebral Microcirculatory Changes in Transient Forebrain Ischemia in Rats: Involvement of Type I Nitric Oxide Synthase." Journal of Cerebral Blood Flow & Metabolism 20, no. 12 (December 2000): 1648–58. http://dx.doi.org/10.1097/00004647-200012000-00004.
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The diameter of surface microvessels and the erythrocyte velocity and flux through intraparenchymal capillaries in the parietal cortex were measured during transient global cerebral ischemia and reperfusion using laser-scanning confocal fluorescence microscopy in anesthetized rats. The role of nitric oxide (NO) from neurons in the microcirculatory changes was also investigated using 7-nitro-indazole (7-NI, 25 mg/kg, IP). Wistar rats (4 per group) equipped with a closed cranial window were given fluorescein isothiocyanate (FITC)-Dextran and FITC-labeled erythrocytes intravenously to respectively visualize the microvessels and the erythrocytes in the capillaries. Experiments were videorecorded on-line. Forebrains were made ischemic for 15 minutes and then reperfused for 120 minutes under the microscope. Ischemia was associated with a flattened EEG, a low persistent blood flow, and a transient leakage of fluorescein across the arteriole wall. Unclamping the carotid arteries led to immediate high blood flow in the arterioles, but it was not until 5 minutes later that the arterioles dilated significantly (181% ± 27%) and erythrocyte velocity in the capillaries increased significantly (460% ± 263%). Neither nonperfused capillaries nor erythrocyte capillary recruitment occurred. 7-Nitro-indazole significantly reduced the arteriole dilatation and prevented the increase in erythrocyte velocity and flux through capillaries in early reperfusion. 7-Nitro-indazole had no influence on the fluorescein leakage. The current study suggests a partial role for NO released from neurons in the postischemic microcirculatory changes and provides new findings on the timing of arteriole dilatation and blood—brain barrier opening, and on erythrocyte capillary circulation in global ischemia.
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Horiuchi, Tetsuyoshi, Hans H. Dietrich, Shinichiro Tsugane, and Ralph G. Dacey. "Analysis of purine- and pyrimidine-induced vascular responses in the isolated rat cerebral arteriole." American Journal of Physiology-Heart and Circulatory Physiology 280, no. 2 (February 1, 2001): H767—H776. http://dx.doi.org/10.1152/ajpheart.2001.280.2.h767.
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Effects of extraluminal UTP were studied and compared with vascular responses to ATP and its analogs in rat cerebral-penetrating arterioles. UTP, UDP, 2-methylthio-ATP, and α,β-methylene-ATP dilated arterioles at the lowest concentration and constricted them at high concentrations. Low concentrations of ATP dilated the vessels; high concentrations caused a biphasic response, with transient constriction followed by dilation. Endothelial impairment inhibited ATP- and UTP-mediated dilation and potentiated constriction to UTP but not to ATP. ATP- and 2-methylthio-ATP- but not UTP-mediated constrictions were inhibited by desensitization with 10−6M α,β-methylene-ATP or 3 × 10−6M pyridoxal phosphate-6-azophenyl-2′,4′-disulfonic acid (PPADS). PPADS at 10−4M abolished the UTP-mediated constriction and induced vasodilation in a dose-dependent manner but did not affect the dilation to ATP. These results suggest that in rat cerebral microvessels 1) ATP and 2-methylthio-ATP induce transient constriction via smooth muscle P2X1receptors in the cerebral arteriole, 2) UTP stimulates two different classes of P2Yreceptors, resulting in constriction (smooth muscle P2Y4) and dilation (possibly endothelial P2Y2), and 3) ATP and UTP produce dilation by stimulation of a single receptor (P2Y2).
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Diaz-Otero, Janice M., Ting-Chieh Yen, Courtney Fisher, Daniel Bota, William F. Jackson, and Anne M. Dorrance. "Mineralocorticoid receptor antagonism improves parenchymal arteriole dilation via a TRPV4-dependent mechanism and prevents cognitive dysfunction in hypertension." American Journal of Physiology-Heart and Circulatory Physiology 315, no. 5 (November 1, 2018): H1304—H1315. http://dx.doi.org/10.1152/ajpheart.00207.2018.
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Hypertension and mineralocorticoid receptor activation cause cerebral parenchymal arteriole remodeling; this can limit cerebral perfusion and contribute to cognitive dysfunction. We used a mouse model of angiotensin II-induced hypertension to test the hypothesis that mineralocorticoid receptor activation impairs both transient receptor potential vanilloid (TRPV)4-mediated dilation of cerebral parenchymal arterioles and cognitive function. Mice (16−18 wk old, male, C57Bl/6) were treated with angiotensin II (800 ng·kg−1·min−1) with or without the mineralocorticoid receptor antagonist eplerenone (100 mg·kg−1·day−1) for 4 wk; sham mice served as controls. Data are presented as means ± SE; n = 5–14 mice/group. Eplerenone prevented the increased parenchymal arteriole myogenic tone and impaired carbachol-induced (10−9–10−5 mol/l) dilation observed during hypertension. The carbachol-induced dilation was endothelium-derived hyperpolarization mediated because it could not be blocked by N-nitro-l-arginine methyl ester (10−5 mol/l) and indomethacin (10−4 mol/l). We used GSK2193874 (10−7 mol/l) to confirm that in all groups this dilation was dependent on TRPV4 activation. Dilation in response to the TRPV4 agonist GSK1016790A (10−9–10−5 mol/l) was also reduced in hypertensive mice, and this defect was corrected by eplerenone. In hypertensive and eplerenone-treated animals, TRPV4 inhibition reduced myogenic tone, an effect that was not observed in arterioles from control animals. Eplerenone treatment also improved cognitive function and reduced microglia density in hypertensive mice. These data suggest that the mineralocorticoid receptor is a potential therapeutic target to improve cerebrovascular function and cognition during hypertension. NEW & NOTEWORTHY Vascular dementia is a growing public health issue that lacks effective treatments. Transient receptor potential vanilloid (TRPV)4 channels are important regulators of parenchymal arteriole dilation, and they modulate myogenic tone. The data presented here suggest that TRPV4 channel expression is regulated by the mineralocorticoid receptor (MR). MR blockade also improves cognitive function during hypertension. MR blockade might be a potential therapeutic approach to improve cerebrovascular function and cognition in patients with hypertension.
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Copeland, J. R., K. A. Willoughby, T. M. Tynan, S. F. Moore, and E. F. Ellis. "Endothelial and nonendothelial cyclooxygenase mediate rabbit pial arteriole dilation by bradykinin." American Journal of Physiology-Heart and Circulatory Physiology 268, no. 1 (January 1, 1995): H458—H466. http://dx.doi.org/10.1152/ajpheart.1995.268.1.h458.
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Aspirin (acetylsalicylic acid, ASA) was administered to rabbits in an attempt to inhibit selectively endothelial cyclooxygenase activity and therefore to determine its role in bradykinin-induced radical-mediated dilation of cerebral arterioles. With the use of the cranial window technique in anesthetized rabbits, pial arteriolar diameters were recorded in response to topically applied bradykinin, acetylcholine, and ventilation with 10% O2-9% CO2 gas mixture. Prostaglandins were measured in isolated cerebral microvessels and cerebrospinal fluid (CSF) using radioimmunoassay. Microvessel prostaglandin production was reduced significantly by 90 mg/kg i.v. ASA, whereas acetylcholine-stimulated increases of CSF prostaglandins were not similarly affected. This treatment reduced bradykinin-induced dilation of pial arterioles by 47%. After concurrent 90 mg/kg i.v. ASA plus 300 microM ASA topically applied to the brain, stimulated increases of CSF prostaglandins were reduced by 79%, while bradykinin-induced dilation was reduced by 78%. ASA did not reduce the dilator activity of either acetylcholine or ventilation with 10% O2-9% CO2. Acetylcholine- but not bradykinin-induced dilation was reduced by NG-nitro-L-arginine methyl ester. These results indicate intravenous ASA produced a relatively selective inhibition of cerebral microvascular cyclooxygenase and partial inhibition of bradykinin-induced dilation. Further inhibition of dilation occurred following ASA administered both systemically and topically to the brain. This indicates two sources of cyclooxygenase, endothelial and nonendothelial, mediate the bradykinin-induced dilation of rabbit pial arterioles. Furthermore, systemic doses of ASA do not eliminate brain prostaglandin formation.
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TULLY, B., and Y. VENTIKOS. "Cerebral water transport using multiple-network poroelastic theory: application to normal pressure hydrocephalus." Journal of Fluid Mechanics 667 (November 16, 2010): 188–215. http://dx.doi.org/10.1017/s0022112010004428.
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The twenty-first century is bearing witness to a drastic change in population demographics and diseases of old age, such as dementia, are placing an unprecedented burden on the global healthcare system. Normal pressure hydrocephalus may be the only curable form of dementia, yet its pathophysiology is paradoxical and a consistent treatment currently remains elusive. A novel application of multiple-network poroelastic theory (MPET) is proposed to investigate water transport in the cerebral environment. Specifically, MPET is modified to allow a detailed investigation of spatio-temporal transport of fluid between the cerebral blood, cerebrospinal fluid (CSF) and brain parenchyma across scales. This framework thus allows an exploration of hypotheses defining the initiation and progression of both acute and chronic hydrocephalus. Results show that a breakdown in the transport mechanisms between the arterial vascular network and interstitial space within the parenchyma may be a cause of accumulation of CSF in the ventricles. Specifically, there must be an increase in the compliance of the arteriole/capillary network, which may combine with a breakdown in the blood–CSF barrier to allow an increased flow from the arteriole/capillary blood to the CSF. The results of this study should prove useful to guide experimental exploration in areas that warrant further investigation and validation.
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Liang, Guo Hua, Qi Xi, Charles W. Leffler, and Jonathan H. Jaggar. "Hydrogen sulfide activates Ca2+sparks to induce cerebral arteriole dilatation." Journal of Physiology 590, no. 11 (May 31, 2012): 2709–20. http://dx.doi.org/10.1113/jphysiol.2011.225128.
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Sharan, Maithili, Eugene P. Vovenko, Arjun Vadapalli, Aleksander S. Popel, and Roland N. Pittman. "Experimental and Theoretical Studies of Oxygen Gradients in Rat Pial Microvessels." Journal of Cerebral Blood Flow & Metabolism 28, no. 9 (May 28, 2008): 1597–604. http://dx.doi.org/10.1038/jcbfm.2008.51.
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Using modified oxygen needle microelectrodes and intravital videomicroscopy, measurements were made of tissue oxygen tension (PO2) profiles near cortical arterioles and transmural PO2 gradients in the pial arterioles of the rat. Under control conditions, the transmural PO2 gradient averaged 1.17 ± 0.06 mm Hg/μm (mean ± s.e., n = 40). Local arteriolar dilation resulted in a marked decrease in the transmural PO2 gradient to 0.68 ± 0.04 mm Hg/μm ( P < 0.001, n = 38). The major finding of this study is a dependence of the transmural PO2 gradient on the vascular tone of the pial arterioles. Using a model of oxygen transport in an arteriole and experimental PO2 profiles, values of radial perivascular and intravascular O2 fluxes were estimated. Our theoretical estimates show that oxygen flux values at the outer surface of the arteriolar wall are approximately 10−5mL O2/cm2 per sec, independent of the values of the arteriolar wall O2 consumption within a wide range of consumption values. This also means that PO2 transmural gradients for cerebral arterioles are within the limits of 1 to 2 mm Hg/μm. The data lead to the conclusion that O2 consumption of the arteriolar wall is within the range for the surrounding tissue and O2 consumption of the endothelial layer appears to have no substantial impact on the transmural PO2 gradient.
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Li, Yao, and Joseph E. Brayden. "Rho kinase activity governs arteriolar myogenic depolarization." Journal of Cerebral Blood Flow & Metabolism 37, no. 1 (July 22, 2016): 140–52. http://dx.doi.org/10.1177/0271678x15621069.
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Cerebral arterioles contribute critically to regulation of local and global blood flow within the brain. Dysfunction of these blood vessels is implicated in numerous cardiovascular diseases. However, treatments are limited due to incomplete understanding of fundamental control mechanisms at this level of circulation. Emerging evidence points to a key role of Rho-associated protein kinase in regulation of microvascular contractility. This study sought to decipher the mechanisms of Rho-associated protein kinase–mediated myogenic vasoconstriction in cerebral parenchymal arterioles. Here, we report that the Rho-associated protein kinase inhibitor H1152 strongly attenuated pressure-induced constriction, cytosolic [Ca2+] increases, and depolarization of isolated parenchymal arterioles. Further, the RhoA activator CN03 potentiated parenchymal arteriole myogenic constriction and depolarization, indicating important involvement of RhoA/Rho-associated protein kinase signaling in myogenic excitation-contraction mechanisms. Because of the well-established role of TRPM4 in pressure-induced depolarization, possible modulatory effects of Rho-associated protein kinase on TRPM4 currents were explored using patch clamp electrophysiology. TRPM4 currents were suppressed by H1152 and enhanced by CN03. Finally, H1152 elevated the apparent [Ca2+]-threshold for TRPM4 activation, suggesting that Rho-associated protein kinase activates TRPM4 by increasing its Ca2+-sensitivity. Our results support a novel mechanism whereby Rho-associated protein kinase–mediated myogenic vasoconstriction occurs primarily through activation of TRPM4 channels, smooth muscle depolarization, and cytosolic [Ca2+] increases in cerebral arterioles.
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Liang, Guohua, Qi xi, Charles Leffler, and Jonathan Jaggar. "P6 Hydrogen sulfide activates Ca2+ sparks to induce cerebral arteriole dilation." Nitric Oxide 27 (September 2012): S13—S14. http://dx.doi.org/10.1016/j.niox.2012.08.007.
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Bauser-Heaton, Holly D., and H. Glenn Bohlen. "Cerebral microvascular dilation during hypotension and decreased oxygen tension: a role for nNOS." American Journal of Physiology-Heart and Circulatory Physiology 293, no. 4 (October 2007): H2193—H2201. http://dx.doi.org/10.1152/ajpheart.00190.2007.
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Endothelial (eNOS) and neuronal nitric oxide synthase (nNOS) are implicated as important contributors to cerebral vascular regulation through nitric oxide (NO). However, direct in vivo measurements of NO in the brain have not been used to dissect their relative roles, particularly as related to oxygenation of brain tissue. We found that, in vivo, rat cerebral arterioles had increased NO concentration ([NO]) and diameter at reduced periarteriolar oxygen tension (Po2) when either bath oxygen tension or arterial pressure was decreased. Using these protocols with highly selective blockade of nNOS, we tested the hypothesis that brain tissue nNOS could donate NO to the arterioles at rest and during periods of reduced perivascular oxygen tension, such as during hypotension or reduced local availability of oxygen. The decline in periarteriolar Po2 by bath manipulation increased [NO] and vessel diameter comparable with responses at similarly decreased Po2 during hypotension. To determine whether the nNOS provided much of the vascular wall NO, nNOS was locally suppressed with the highly selective inhibitor N-(4S)-(4-amino-5-[aminoethyl]aminopentyl)- N′-nitroguanidine. After blockade, resting [NO], Po2, and diameters decreased, and the increase in [NO] during reduced Po2 or hypotension was completely absent. However, flow-mediated dilation during occlusion of a collateral arteriole did remain intact after nNOS blockade and the vessel wall [NO] increased to ∼80% of normal. Therefore, nNOS predominantly increased NO during decreased periarteriolar oxygen tension, such as that during hypotension, but eNOS was the dominant source of NO for flow shear mechanisms.
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Hauck, Erik F., Sebastian Apostel, Julie F. Hoffmann, Axel Heimann, and Oliver Kempski. "Capillary Flow and Diameter Changes during Reperfusion after Global Cerebral Ischemia Studied by Intravital Video Microscopy." Journal of Cerebral Blood Flow & Metabolism 24, no. 4 (April 2004): 383–91. http://dx.doi.org/10.1097/00004647-200404000-00003.
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The reaction of cerebral capillaries to ischemia is unclear. Based on Hossmann's observation of postischemic “delayed hypoperfusion,” we hypothesized that capillary flow is decreased during reperfusion because of increased precapillary flow resistance. To test this hypothesis, we measured cerebral capillary erythrocyte velocity and diameter changes by intravital microscopy in gerbils. A cranial window was prepared over the frontoparietal cortex in 26 gerbils anesthetized with halothane. The animals underwent either a sham operation or fifteen minutes of bilateral carotid artery occlusion causing global cerebral ischemia. Capillary flow velocities were measured by frame-to-frame tracking of fluorescein isothiocyanate labeled erythrocytes in 1800 capillaries after 1-hour reperfusion. Capillary flow velocities were decreased compared to control (0.25 ± 0.27mm/s vs. 0.76 ± 0.45 mm/s; P < 0.001). Precapillary arteriole diameters in reperfused animals were reduced to 76.3 ± 6.9% compared to baseline ( P < 0.05). Capillary diameters in reperfused animals (2.87 ± 0.97 μm) were reduced ( P < 0.001) compared to control (4.08 ± 1.19 μm). Similar reductions of precapillary (24%) and capillary vessel diameters (30%) and absolute capillary flow heterogeneity indicate that delayed (capillary) hypoperfusion occurs as a consequence of increased precapillary arteriole tone during reperfusion.
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Golding, Elke M., Claudia S. Robertson, Jane C. K. Fitch, J. Clay Goodman, and Robert M. Bryan. "Segmental Vascular Resistance after Mild Controlled Cortical Impact Injury in the Rat." Journal of Cerebral Blood Flow & Metabolism 23, no. 2 (February 2003): 210–18. http://dx.doi.org/10.1097/01.wcb.0000044739.64940.b5.
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In an effort to localize the site at which increased resistance occurs after brain trauma, pial arteriole diameter and pressure were assessed after mild controlled cortical impact (CCI) injury in rats using an open cranial window technique. The authors tested the hypothesis that an increase in resistance accompanied by vasoconstriction occurs at the level of the pial arterioles within the injured cortex of the brain. At 1 hour after mild CCI injury, ipsilateral cerebral blood flow was significantly reduced by 42% compared with sham injury (n = 4; P < 0.05). Pial arteriole diameter and pressure remained unchanged. Resistance in the larger arteries (proximal resistance), however, was significantly greater after CCI injury (1.87 ± 0.26 mm Hg/[mL · 100 g · min]) compared with sham injury (0.91 ± 0.21 mm Hg/[mL · 100 g ·min]; P < 0.0001). Resistance in small vessels, arterioles, and venules (distal resistance) was also significantly greater after CCI injury (1.13 ± 0.05 mm Hg/[mL · 100 g · min]) compared with sham injury (0.74 ± 0.13 mm Hg/[mL · 100 g · min]; P = 0.0001). The authors conclude that, at 1 hour after mild CCI injury, changes in vascular resistance comprise a 53% increase in the resistance distal to the area of injury and, surprisingly, a 105% increase in resistance in the arteries proximal to the injury site.
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Takayasu, Masakazu, and Ralph G. Dacey. "Spontaneous tone of cerebral parenchymal arterioles: a role in cerebral hyperemic phenomena." Journal of Neurosurgery 71, no. 5 (November 1989): 711–17. http://dx.doi.org/10.3171/jns.1989.71.5.0711.
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✓ An isolated cerebral arteriole preparation was used to test the hypothesis that a temporary reduction in transmural pressure causes a subsequent vasodilation mediated by mechanisms intrinsic to the vessel wall. Thirty-five cerebral vessels of 44.7 ± 1.4 µm (± standard error of the mean) mean diameter were cannulated in vitro and pressurized at a transmural pressure of 60 mm Hg; after an equilibration period the vessels developed spontaneous tone. When transmural pressure was decreased to 0 mm Hg for a period of 4 minutes then returned to 60 mm Hg, vessels dilated to 155.1% ± 6.8% of control diameter before gradually redeveloping spontaneous tone in 5.5 ± 0.7 minutes. Varying the duration of the period during which transmural pressure was at 0 mm Hg had no significant effect on the degree of vasodilation. Conversely, varying the level of decreased transmural pressure between 0 and 20 mm Hg significantly affected both the magnitude of vasodilation and the time course of spontaneous tone recovery. These findings indicate that a temporary period of decreased transmural pressure may result in a loss of spontaneous tone in the resistance vessels of the cerebral microcirculation. Mechanisms intrinsic to the vessel wall may play a significant role in the early stage of post-reperfusion hyperemia. Such mechanisms could also be implicated in other hyperemic phenomena affecting the cerebral circulation, such as the rapid increase in intracranial pressure after subarachnoid hemorrhage, the development of the normal perfusion pressure breakthrough phenomenon, and the initiation of intracranial pressure plateau waves.
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Harraz, Osama F., Thomas A. Longden, Fabrice Dabertrand, David Hill-Eubanks, and Mark T. Nelson. "Endothelial GqPCR activity controls capillary electrical signaling and brain blood flow through PIP2 depletion." Proceedings of the National Academy of Sciences 115, no. 15 (March 26, 2018): E3569—E3577. http://dx.doi.org/10.1073/pnas.1800201115.
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Brain capillaries play a critical role in sensing neural activity and translating it into dynamic changes in cerebral blood flow to serve the metabolic needs of the brain. The molecular cornerstone of this mechanism is the capillary endothelial cell inward rectifier K+ (Kir2.1) channel, which is activated by neuronal activity–dependent increases in external K+ concentration, producing a propagating hyperpolarizing electrical signal that dilates upstream arterioles. Here, we identify a key regulator of this process, demonstrating that phosphatidylinositol 4,5-bisphosphate (PIP2) is an intrinsic modulator of capillary Kir2.1-mediated signaling. We further show that PIP2 depletion through activation of Gq protein-coupled receptors (GqPCRs) cripples capillary-to-arteriole signal transduction in vitro and in vivo, highlighting the potential regulatory linkage between GqPCR-dependent and electrical neurovascular-coupling mechanisms. These results collectively show that PIP2 sets the gain of capillary-initiated electrical signaling by modulating Kir2.1 channels. Endothelial PIP2 levels would therefore shape the extent of retrograde signaling and modulate cerebral blood flow.
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Not Available, Not Available. "Astrocytes act as signal transducer in neuronal activation and cerebral arteriole vasodilation." Journal of Neurology 250, no. 3 (March 1, 2003): 384–86. http://dx.doi.org/10.1007/s004150300013.
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Shibata, M., C. W. Leffler, and D. W. Busija. "Prostanoids attenuate pial arteriolar dilation induced by cortical spreading depression in rabbits." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 261, no. 4 (October 1, 1991): R828—R834. http://dx.doi.org/10.1152/ajpregu.1991.261.4.r828.
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The role of prostanoids in mediating cerebrovascular responses to cortical spreading depression (CSD) was examined in anesthetized rabbits. CSD was elicited by KCl microinjection, and its propagation was monitored electrophysiologically. Pial arterial diameter was determined using a closed cranial window and intravital microscopy, and regional cerebral blood flow (rCBF) was determined using laser flowmetry. Levels of peri-arachnoid cerebrospinal fluid prostanoids were determined by radioimmunoassay. CSF increased pial arteriolar diameter 62% and rCBF 354% over the baseline levels. Locations of propagating CSD, dilating pial arteriole, and increased rCBF were always closely associated spatiotemporally. Cerebrospinal fluid prostanoid levels increased during single CSD-induced arteriolar dilation, and they were further augmented during multiple CSDs. Indomethacin enhanced both CSD-induced vasodilation (88%) and rCBF increase (580%), but it decreased the cerebrospinal fluid levels of prostanoids below the baseline levels and prevented their increase during CSD-induced vasodilation. These results indicate that prostanoids are synthesized from neurons or glial cells and/or the brain vessels and, as the net result, counteract pial arteriolar dilation and rCBF increase during CSD. In addition, they support the hypothesis that the vasodilation is caused primarily by neurogenic factors associated with CSD.
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Nakahata, Katsutoshi, Hiroyuki Kinoshita, Yusei Hirano, Yoshiki Kimoto, Hiroshi Iranami, and Yoshio Hatano. "Mild Hypercapnia Induces Vasodilation via Adenosine Triphosphate-sensitive K+Channels in Parenchymal Microvessels of the Rat Cerebral Cortex." Anesthesiology 99, no. 6 (December 1, 2003): 1333–39. http://dx.doi.org/10.1097/00000542-200312000-00014.
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Background Carbon dioxide is an important vasodilator of cerebral blood vessels. Cerebral vasodilation mediated by adenosine triphosphate (ATP)-sensitive K+ channels has not been demonstrated in precapillary microvessel levels. Therefore, the current study was designed to examine whether ATP-sensitive K+ channels play a role in vasodilation induced by mild hypercapnia in precapillary arterioles of the rat cerebral cortex. Methods Brain slices from rat cerebral cortex were prepared and superfused with artificial cerebrospinal fluid, including normal (Pco2 = 40 mmHg; pH = 7.4), hypercapnic (Pco2 = 50 mmHg; pH = 7.3), and hypercapnic normal pH (Pco2 = 50 mmHg; pH = 7.4) solutions. The ID of a cerebral parenchymal arteriole (5-9.5 microm) was monitored using computerized videomicroscopy. Results During contraction to prostaglandin F2alpha (5 x 10(-7) m), hypercapnia, but not hypercapnia under normal pH, induced marked vasodilation, which was completely abolished by the selective ATP-sensitive K+ channel antagonist glibenclamide (5 x 10(-6) m). However, the selective Ca2+-dependent K+ channel antagonist iberiotoxin (10(-7) m) as well as the nitric oxide synthase inhibitor NG-nitro-L-arginine methyl ester (10(-4) m) did not alter vasodilation. A selective ATP-sensitive K+ channel opener, levcromakalim (3 x 10(-8) to 3 x 10(-7) m), induced vasodilation, whereas this vasodilation was abolished by glibenclamide. Conclusion These results suggest that in parenchymal microvessels of the rat cerebral cortex, decreased pH corresponding with hypercapnia, but not hypercapnia itself, contributes to cerebral vasodilation produced by carbon dioxide and that ATP-sensitive K+ channels play a major role in vasodilator responses produced by mild hypercapnia.
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Krsmanovic, Zeljko, Evica Dincic, Smiljana Kostic, Vesna Lackovic, Milos Bajcetic, Maja Lackovic, Zeljko Boskovic, and Ranko Raicevic. "Cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy." Vojnosanitetski pregled 68, no. 5 (2011): 455–59. http://dx.doi.org/10.2298/vsp1105455k.
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Introduction. Fast and precise diagnostics of the disease from the large group of adult leukoencephalopathy is difficult but responsible job, because the outcome of the disease is very often determined by its name. Cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL) is caused by the mutation of Notch 3 gene on chromosome locus 19p13. Beside the brain arterioles being the main disease targets, extracerebral small blood vessels are affected by the pathological process. Clinically present signs are recurrent ischemic strokes and vascular dementia. CADASIL in its progressive form shows a distinctive pattern of pathological changes on MRI of endocranium. The diagnosis is confirmed by the presence of granular osmiophilic material (GOM) in histopathological skin biopsies. Case reports. Two young adult patients manifested ischemic strokes of unknown etiology, cognitive deterioration, migraine and psychopathological phenomenology. MRI of endocranium pointed on CADASIL. Ultrastructural examination of skin biopsy proved the presence of GOM in the basal lamina and near smooth muscle cells of arteriole dermis leading to CADASIL diagnosis. The presence of GOM in histopathological preparation is 100% specific for CADASIL. The patients were not searched for mutation in Notch 3 gene on chromosome 19, because some other leukoencephalopathy was disregarded. Conclusion. Suggestive clinical picture, distinctive finding of endocranium MRI, the presence of GOM by ultrastructural examination of histopathological skin biopsies are sufficient to confirm CADASIL diagnosis.
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Zhao, Dong, Yezhong Wang, Xuejun He, Luna Liu, Qi Liu, Hui Xu, Yunxiang Ji, Licang Zhu, Ganggang Wang, and Jian Xu. "Correlation between Arteriole Membrane Potential and Cerebral Vasospasm after Subarachnoid Hemorrhage in Rats." Neurology India 68, no. 2 (2020): 327. http://dx.doi.org/10.4103/0028-3886.280652.
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Longden, Thomas A., David C. Hill-Eubanks, and Mark T. Nelson. "Ion channel networks in the control of cerebral blood flow." Journal of Cerebral Blood Flow & Metabolism 36, no. 3 (November 9, 2015): 492–512. http://dx.doi.org/10.1177/0271678x15616138.
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One hundred and twenty five years ago, Roy and Sherrington made the seminal observation that neuronal stimulation evokes an increase in cerebral blood flow.1 Since this discovery, researchers have attempted to uncover how the cells of the neurovascular unit—neurons, astrocytes, vascular smooth muscle cells, vascular endothelial cells and pericytes—coordinate their activity to control this phenomenon. Recent work has revealed that ionic fluxes through a diverse array of ion channel species allow the cells of the neurovascular unit to engage in multicellular signaling processes that dictate local hemodynamics. In this review we center our discussion on two major themes: (1) the roles of ion channels in the dynamic modulation of parenchymal arteriole smooth muscle membrane potential, which is central to the control of arteriolar diameter and therefore must be harnessed to permit changes in downstream cerebral blood flow, and (2) the striking similarities in the ion channel complements employed in astrocytic endfeet and endothelial cells, enabling dual control of smooth muscle from either side of the blood–brain barrier. We conclude with a discussion of the emerging roles of pericyte and capillary endothelial cell ion channels in neurovascular coupling, which will provide fertile ground for future breakthroughs in the field.
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Dacey, Ralph G., John E. Bassett, and Masakazu Takayasu. "Vasomotor Responses of Rat Intracerebral Arterioles to Vasoactive Intestinal Peptide, Substance P, Neuropeptide Y, and Bradykinin." Journal of Cerebral Blood Flow & Metabolism 8, no. 2 (April 1988): 254–61. http://dx.doi.org/10.1038/jcbfm.1988.56.
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The effect of vasoactive peptides on vascular smooth muscle in the cerebral microcirculation was examined using an isolated intracerebral arteriole preparation. Extraluminally applied vasoactive intestinal peptide (VIP) dilated the spontaneous tone of intracerebral arterioles to 118.9 ± 3.1% of control diameter at pH 7.30, with an EC50 of 7.27 × 10−8 M. Similar degrees of dilation to VIP were seen in vessels preconstricted by changing bath solution to pH 7.60. Substance P had no effect on vessel diameter at pH 7.30. However, in vessels precontracted by pH 7.60, significant dose-dependent dilation was observed with an EC50 of 2.55 × 10−10 M. Neuropeptide constricted intracerebral arterioles to 8l.22 ± 2.7% of control diameter, with an EC50 of 6.23 × 10−10 M. Bradykinin dilated intracerebral arterioles at pH 7.30 and pH 7.60 to 130 ± 3.0% of control diameter. VIP and bradykinin are potent vasodilators of intracerebral arterioles. Neuropeptide Y is a vasoconstrictor. The effect of substance P appeared to be either pH-dependent or dependent on some degree of precontraction by another agonist, but no effect on vessel diameter was seen at pH 7.30.
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Tóth, Réka, Attila E. Farkas, István A. Krizbai, Péter Makra, Ferenc Bari, Eszter Farkas, and Ákos Menyhárt. "Astrocyte Ca2+ Waves and Subsequent Non-Synchronized Ca2+ Oscillations Coincide with Arteriole Diameter Changes in Response to Spreading Depolarization." International Journal of Molecular Sciences 22, no. 7 (March 26, 2021): 3442. http://dx.doi.org/10.3390/ijms22073442.
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Spreading depolarization (SD) is a wave of mass depolarization that causes profound perfusion changes in acute cerebrovascular diseases. Although the astrocyte response is secondary to the neuronal depolarization with SD, it remains to be explored how glial activity is altered after the passage of SD. Here, we describe post-SD high frequency astrocyte Ca2+ oscillations in the mouse somatosensory cortex. The intracellular Ca2+ changes of SR101 labeled astrocytes and the SD-related arteriole diameter variations were simultaneously visualized by multiphoton microscopy in anesthetized mice. Post-SD astrocyte Ca2+ oscillations were identified as Ca2+ events non-synchronized among astrocytes in the field of view. Ca2+ oscillations occurred minutes after the Ca2+ wave of SD. Furthermore, fewer astrocytes were involved in Ca2+ oscillations at a given time, compared to Ca2+ waves, engaging all astrocytes in the field of view simultaneously. Finally, our data confirm that astrocyte Ca2+ waves coincide with arteriolar constriction, while post-SD Ca2+ oscillations occur with the peak of the SD-related vasodilation. This is the first in vivo study to present the post-SD astrocyte Ca2+ oscillations. Our results provide novel insight into the spatio-temporal correlation between glial reactivity and cerebral arteriole diameter changes behind the SD wavefront.
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Zhang, Hua, Pranay Prabhakar, Robert Sealock, and James E. Faber. "Wide Genetic Variation in the Native Pial Collateral Circulation is a Major Determinant of Variation in Severity of Stroke." Journal of Cerebral Blood Flow & Metabolism 30, no. 5 (February 3, 2010): 923–34. http://dx.doi.org/10.1038/jcbfm.2010.10.
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Severity of stroke varies widely among individuals. Whether differences in the extent of the native (preexisting) pial collateral circulation exist and contribute to this variability is unknown. We addressed these questions and probed for potential genetic contributions using morphometric analysis of the collateral circulation in 15 inbred mouse strains recently shown to exhibit wide differences in infarct volume. Morphometrics were determined in the unligated left hemisphere (for native collaterals) and ligated right hemisphere (for remodeled collaterals) 6 days after permanent middle cerebral artery (MCA) occlusion. Variation among strains in native collateral number, diameter, MCA, anterior cerebral artery (ACA), and posterior cerebral artery (PCA) tree territories were, respectively: 56-fold, 3-fold, 42%, 56%, and 61%. Collateral length ( P<0.001) and the number of penetrating arterioles branching from them also varied ( P<0.05). Infarct volume correlated inversely with collateral number ( P<0.0001), diameter ( P<0.0001), and penetrating arteriole number ( P<0.05) and directly with MCA territory ( P<0.05). Relative collateral conductance and MCA territory, when factored together, strongly predicted infarct volume ( P<0.0001). Outward remodeling of collaterals in the ligated hemisphere varied ∼3-fold. These data show that the extent of the native pial collateral circulation and collateral remodeling after obstruction vary widely with genetic background, and suggest that this variability, due to natural polymorphisms, is a major contributor to variability in infarct volume.
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Migrino, Raymond Q., Seth Truran, Nina Karamanova, Geidy E. Serrano, Calvin Madrigal, Hannah A. Davies, Jillian Madine, Peter Reaven, and Thomas G. Beach. "Human cerebral collateral arteriole function in subjects with normal cognition, mild cognitive impairment, and dementia." American Journal of Physiology-Heart and Circulatory Physiology 315, no. 2 (August 1, 2018): H284—H290. http://dx.doi.org/10.1152/ajpheart.00206.2018.
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Clinical and preclinical studies have suggested a link between cardiovascular disease and dementia disorders, but the role of the collateral brain circulation in cognitive dysfunction remains unknown. We aimed to test the hypothesis that leptomeningeal arteriole (LMA) function and response to metabolic stressors differ among subjects with dementia, mild cognitive impairment (MCI), and normal cognition (CN). After rapid autopsy, LMAs were isolated from subjects with CN ( n = 10), MCI ( n = 12), or dementia [ n = 42, Alzheimer’s disease (AD), vascular dementia (VaD), or other dementia], and endothelial and smooth muscle-dependent function were measured at baseline and after exposure to β-amyloid (2 μM), palmitic acid (150 μM), or medin (5 μM) and compared. There were no differences among the groups in baseline endothelial function (maximum dilation to acetylcholine, CN: 74.1 ± 9.7%, MCI: 67.1 ± 4.8%, AD: 74.7 ± 2.8%, VaD: 72.0 ± 5.3%, and other dementia: 68.0 ± 8.0%) and smooth muscle-dependent function (CN: 93.4 ± 3.0%, MCI: 83.3 ± 4.1%, AD: 91.8 ± 1.7%, VaD: 91.7 ± 2.4%, and other dementia: 87.9 ± 4.9%). There was no correlation between last cognitive function score and baseline endothelial or smooth muscle-dependent function. LMA endothelial function and, to a lesser extent, smooth muscle-dependent function were impaired posttreatment with β-amyloid, palmitic acid, and medin. Posttreatment LMA responses were not different between subjects with CN/MCI vs. dementia. Baseline responses and impaired vasoreactivity after treatment with metabolic stressors did not differ among subjects with CN, MCI, and dementia. The results suggest that the cognitive dysfunction in dementia disorders is not attributable to differences in baseline brain collateral circulation function but may be influenced by exposure of the vasculature to metabolic stressors. NEW & NOTEWORTHY Here, we present novel findings that brain collateral arteriole function did not differ among subjects with normal cognition, mild cognitive impairment, and dementia (Alzheimer’s disease and vascular dementia). Although arteriole function was impaired by vascular stressors (β-amyloid, palmitic acid, and medin), responses did not differ between those with or without dementia. The cognitive dysfunction in dementia disorders is not attributable to differences in baseline brain collateral circulation function but may be influenced by vascular exposure to metabolic stressors.
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Pritchard, Harry A. T., Paulo W. Pires, Evan Yamasaki, Pratish Thakore, and Scott Earley. "Nanoscale remodeling of ryanodine receptor cluster size underlies cerebral microvascular dysfunction in Duchenne muscular dystrophy." Proceedings of the National Academy of Sciences 115, no. 41 (September 4, 2018): E9745—E9752. http://dx.doi.org/10.1073/pnas.1804593115.
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Duchenne muscular dystrophy (DMD) results from mutations in the gene encoding dystrophin which lead to impaired function of skeletal and cardiac muscle, but little is known about the effects of the disease on vascular smooth muscle cells (SMCs). Here we used the mdx mouse model to study the effects of mutant dystrophin on the regulation of cerebral artery and arteriole SMC contractility, focusing on an important Ca2+-signaling pathway composed of type 2 ryanodine receptors (RyR2s) on the sarcoplasmic reticulum (SR) and large-conductance Ca2+-activated K+ (BK) channels on the plasma membrane. Nanoscale superresolution image analysis revealed that RyR2 and BKα were organized into discrete clusters, and that the mean size of RyR2 clusters that colocalized with BKα was larger in SMCs from mdx mice (∼62 RyR2 monomers) than in controls (∼40 RyR2 monomers). We further found that the frequency and signal mass of spontaneous, transient Ca2+-release events through SR RyR2s (“Ca2+ sparks”) were greater in SMCs from mdx mice. Patch-clamp electrophysiological recordings indicated a corresponding increase in Ca2+-dependent BK channel activity. Using pressure myography, we found that cerebral pial arteries and parenchymal arterioles from mdx mice failed to develop appreciable spontaneous myogenic tone. Inhibition of RyRs with tetracaine and blocking of BK channels with paxilline restored myogenic tone to control levels, demonstrating that enhanced RyR and BK channel activity is responsible for the diminished pressure-induced constriction of arteries and arterioles from mdx mice. We conclude that increased size of RyR2 protein clusters in SMCs from mdx mice increases Ca2+ spark and BK channel activity, resulting in cerebral microvascular dysfunction.
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Taylor, Zachary J., Edward S. Hui, Ashley N. Watson, Xingju Nie, Rachael L. Deardorff, Jens H. Jensen, Joseph A. Helpern, and Andy Y. Shih. "Microvascular basis for growth of small infarcts following occlusion of single penetrating arterioles in mouse cortex." Journal of Cerebral Blood Flow & Metabolism 36, no. 8 (October 13, 2015): 1357–73. http://dx.doi.org/10.1177/0271678x15608388.
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Small cerebral infarcts, i.e. microinfarcts, are common in the aging brain and linked to vascular cognitive impairment. However, little is known about the acute growth of these minute lesions and their effect on blood flow in surrounding tissues. We modeled microinfarcts in the mouse cortex by inducing photothrombotic clots in single penetrating arterioles. The resultant hemodynamic changes in tissues surrounding the occluded vessel were then studied using in vivo two-photon microscopy. We were able to generate a spectrum of infarct volumes by occluding arterioles that carried a range of blood fluxes. Those resulting from occlusion of high-flux penetrating arterioles (flux of 2 nL/s or higher) exhibited a radial outgrowth that encompassed unusually large tissue volumes. The gradual expansion of these infarcts was propagated by an evolving insufficiency in capillary flow that encroached on territories of neighboring penetrating arterioles, leading to the stagnation and recruitment of their perfusion domains into the final infarct volume. Our results suggest that local collapse of microvascular function contributes to tissue damage incurred by single penetrating arteriole occlusions in mice, and that a similar mechanism may add to pathophysiology induced by microinfarcts of the human brain.
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Rupin, Alain, Frédéric Martin, Marie-Odile Vallez, Edith Bonhomme, and Tony Verbeuren. "Inactivation of Plasminogen Activator Inhibitor-1 Accelerates Thrombolysis of a Platelet-rich Thrombus in Rat Mesenteric Arterioles." Thrombosis and Haemostasis 86, no. 12 (2001): 1528–31. http://dx.doi.org/10.1055/s-0037-1616758.
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SummaryTo investigate the role of active plasminogen activator inhibitor 1 (PAI-1) in the evolution of a microthrombus generated in the arteriolar microcirculation, the monoclonal antibody, 33H1F7, which transforms active PAI-1 to a tissue type plasminogen activator (t-PA) substrate, was evaluated in an arteriolar thrombosis model in the rat mesentery. Arterioles (200-300 μm) were stimulated electrically to create an endothelial lesion; ADP was then perfused for 2 min to induce the formation of a platelet-rich thrombus which lysed spontaneously in 140 ± 24 s. Two successive ADP superfusions produced comparable thrombi which lysed in comparable times. Different doses of 33H1F7 were infused to rats for 30 min and the dose which inactivates rapidly and totally active rat PAI-1 (300 μg/kg/min) was selected to be tested on the thrombosis model. Infusion of 33H1F7 beginning 10 min before the ADP application significantly reduced the lysis time in comparison to the control (123 ± 30 s versus 169 ± 33 s, P < 0.05, paired Student’s t-test) and the cumulative thrombus area during the lysis period was decreased by 56 ± 7%. These results demonstrate that inactivation of PAI-1 is able to accelerate lysis of a platelet-rich clot in a mesenteric arteriole of the rat. Thus active PAI-1 most likely participates to the resistance to thrombolysis in the arteriolar microcirculation and its inactivation may shorten ischemic periods after microvascular obstruction such as e.g. during cerebral stroke.
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el Gibaly, Ahmed, Omar A. El-Bassiouny, Omar Diaa, Ali I. Shehata, Tamer Hassan, and Khalid M. Saqr. "Effects of Non-Newtonian Viscosity on the Hemodynamics of Cerebral Aneurysms." Applied Mechanics and Materials 819 (January 2016): 366–70. http://dx.doi.org/10.4028/www.scientific.net/amm.819.366.
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The purpose of this study is to present a comparative study between Newtonian and non-Newtonian blood viscosity models for simulating the hemodynamic wall shear stress (WSS) of cerebral aneurysms. The non-Newtonian blood viscosity was modeled using the Carreau-Yasuda nonlinear model. Two realistic cerebral aneurysm models, derived from 3D angiography imaging, were studied and simulated via computational fluid dynamics solver based on finite volume method, with a pulsating sinusoidal waveform boundary conditions. The maximum wall shear stresses were found at the aneurysm’s neck and apex, the inlet arteriole recorded an average wall shear stress and as for the blebs and tips the wall shear stress values were remarkably low. The comparison indicated that non-Newtonian blood viscosity model predicted a lower range of WSS than of the Newtonian model, which provides more accuracy for simulating aneurysm hemodynamics.
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Misaki, Toshinari, Yoh-ichi Satoh, Tomoyuki Saino, Takashi Kuroda, Kazuki Masu, D. A. Russa, and Akira Ogawa. "Immunohistochemical localization of protease-activated receptors in cerebral and testicular arterioles of rats: their dependence on arteriole size and organ-specificity." Archives of Histology and Cytology 71, no. 3 (2008): 179–84. http://dx.doi.org/10.1679/aohc.71.179.
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Haydon, Philip G., and Giorgio Carmignoto. "Astrocyte Control of Synaptic Transmission and Neurovascular Coupling." Physiological Reviews 86, no. 3 (July 2006): 1009–31. http://dx.doi.org/10.1152/physrev.00049.2005.
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From a structural perspective, the predominant glial cell of the central nervous system, the astrocyte, is positioned to regulate synaptic transmission and neurovascular coupling: the processes of one astrocyte contact tens of thousands of synapses, while other processes of the same cell form endfeet on capillaries and arterioles. The application of subcellular imaging of Ca2+ signaling to astrocytes now provides functional data to support this structural notion. Astrocytes express receptors for many neurotransmitters, and their activation leads to oscillations in internal Ca2+. These oscillations induce the accumulation of arachidonic acid and the release of the chemical transmitters glutamate, d-serine, and ATP. Ca2+ oscillations in astrocytic endfeet can control cerebral microcirculation through the arachidonic acid metabolites prostaglandin E2 and epoxyeicosatrienoic acids that induce arteriole dilation, and 20-HETE that induces arteriole constriction. In addition to actions on the vasculature, the release of chemical transmitters from astrocytes regulates neuronal function. Astrocyte-derived glutamate, which preferentially acts on extrasynaptic receptors, can promote neuronal synchrony, enhance neuronal excitability, and modulate synaptic transmission. Astrocyte-derived d-serine, by acting on the glycine-binding site of the N-methyl-d-aspartate receptor, can modulate synaptic plasticity. Astrocyte-derived ATP, which is hydrolyzed to adenosine in the extracellular space, has inhibitory actions and mediates synaptic cross-talk underlying heterosynaptic depression. Now that we appreciate this range of actions of astrocytic signaling, some of the immediate challenges are to determine how the astrocyte regulates neuronal integration and how both excitatory (glutamate) and inhibitory signals (adenosine) provided by the same glial cell act in concert to regulate neuronal function.
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Kimura, M., H. H. Dietrich, V. H. Huxley, D. R. Reichner, and R. G. Dacey. "Measurement of hydraulic conductivity in isolated arterioles of rat brain cortex." American Journal of Physiology-Heart and Circulatory Physiology 264, no. 6 (June 1, 1993): H1788—H1797. http://dx.doi.org/10.1152/ajpheart.1993.264.6.h1788.
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We have developed a new method for quantification of arteriolar hydraulic conductivity (Lp) from isolated rat brain vessels. The volume flux of water per unit surface area across the arteriole wall (Jv/S) was assessed from measurements of silicon oil drop movement within an occluded vessel at two to three pressures (between 20 and 70 mmHg); the Lp was derived from the slope of the relationship between Jv/S and applied pressure. Lp was measured in isolated cerebral arterioles 1) at room temperature (22 degrees C) without spontaneous vessel tone (control Lp; n = 11), 2) at room temperature with 10(-4) M adenosine (n = 5), and 3) at 37 degrees C with vessels dilated submaximally with 10(-4) M adenosine (n = 6). Lp at 22 degrees C without adenosine was 13.2 +/- 4.2 x 10(-9) (+/- SE) cm.s-1.cmH2O-1 for all vessels studied. Lp values ranged from 1.2 to 44.1 x 10(-9) cm.s-1.cmH2O-1 with a median value that was 5.9 x 10(-9) cm.s-1.cmH2O-1. Lp increased significantly (on average, 2.6-fold) with adenosine at 37 degrees C but not with adenosine at 22 degrees C. Control Lp bore no relationship to either the development of spontaneous tone or the diameter response to pH change, two recognized indicators of vessel viability.
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Staehr, Christian, Rajkumar Rajanathan, Dmitry D. Postnov, Lise Hangaard, Elena V. Bouzinova, Karin Lykke-Hartmann, Flemming W. Bach, Shaun L. Sandow, Christian Aalkjaer, and Vladimir V. Matchkov. "Abnormal neurovascular coupling as a cause of excess cerebral vasodilation in familial migraine." Cardiovascular Research 116, no. 12 (November 9, 2019): 2009–20. http://dx.doi.org/10.1093/cvr/cvz306.
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Abstract Aims Acute migraine attack in familial hemiplegic migraine type 2 (FHM2) patients is characterized by sequential hypo- and hyperperfusion. FHM2 is associated with mutations in the Na, K-ATPase α2 isoform. Heterozygous mice bearing one of these mutations (α2+/G301R mice) were shown to have elevated cerebrovascular tone and, thus, hypoperfusion that might lead to elevated concentrations of local metabolites. We hypothesize that these α2+/G301R mice also have increased cerebrovascular hyperaemic responses to these local metabolites leading to hyperperfusion in the affected part of the brain. Methods and results Neurovascular coupling was compared in α2+/G301R and matching wild-type (WT) mice using Laser Speckle Contrast Imaging. In brain slices, parenchymal arteriole diameter and intracellular calcium changes in neuronal tissue, astrocytic endfeet, and smooth muscle cells in response to neuronal excitation were assessed. Wall tension and smooth muscle membrane potential were measured in isolated middle cerebral arteries. Quantitative polymerase chain reaction, western blot, and immunohistochemistry were used to assess the molecular background underlying the functional changes. Whisker stimulation induced larger increase in blood perfusion, i.e. hyperaemic response, of the somatosensory cortex of α2+/G301R than WT mice. Neuronal excitation was associated with larger parenchymal arteriole dilation in brain slices from α2+/G301R than WT mice. These hyperaemic responses in vivo and ex vivo were inhibited by BaCl2, suggesting involvement of inward-rectifying K+ channels (Kir). Relaxation to elevated bath K+ was larger in arteries from α2+/G301R compared to WT mice. This difference was endothelium-dependent. Endothelial Kir2.1 channel expression was higher in arteries from α2+/G301R mice. No sex difference in functional responses and Kir2.1 expression was found. Conclusion This study suggests that an abnormally high cerebrovascular hyperaemic response in α2+/G301R mice is a result of increased endothelial Kir2.1 channel expression. This may be initiated by vasospasm-induced accumulation of local metabolites and underlie the hyperperfusion seen in FHM2 patients during migraine attack.
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Diaz-Otero, Janice M., Courtney Fisher, Kelsey Downs, M. Elizabeth Moss, Iris Z. Jaffe, William F. Jackson, and Anne M. Dorrance. "Endothelial Mineralocorticoid Receptor Mediates Parenchymal Arteriole and Posterior Cerebral Artery Remodeling During Angiotensin II–Induced Hypertension." Hypertension 70, no. 6 (December 2017): 1113–21. http://dx.doi.org/10.1161/hypertensionaha.117.09598.
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Baumbach, G. L., J. E. Siems, F. M. Faraci, and D. D. Heistad. "Mechanics and composition of arterioles in brain stem and cerebrum." American Journal of Physiology-Heart and Circulatory Physiology 256, no. 2 (February 1, 1989): H493—H501. http://dx.doi.org/10.1152/ajpheart.1989.256.2.h493.
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The goal of this study was to compare mechanics and composition of arterioles in brain stem and cerebrum. We calculated stress and strain of pial arterioles in anesthetized rats from measurements of pial arteriolar pressure (servo-null), diameter, and cross-sectional area of the vessel wall. Composition of pial arterioles was quantitated using point-counting stereology. Before deactivation of smooth muscle with ethylenediaminetetraacetic acid (EDTA), pial arteriolar pressure and diameter were 28 and 30% greater (P less than 0.05) in brain stem than cerebrum. After EDTA, diameter of arterioles was similar in brain stem and cerebrum. Cross-sectional area of the arteriolar wall was 32% greater (P less than 0.05) in brain stem than cerebrum. Stress-strain curves indicated that distensibility of pial arterioles is greater in brain stem than cerebrum. The proportion of nondistensible (collagen and basement membrane) to distensible (elastin, smooth muscle, and endothelium) components was 20% less (P less than 0.05) in brain stem than cerebral arterioles. We conclude that 1) cross-sectional area of the vessel wall in arterioles of comparable size is greater in brain stem than cerebrum, 2) distensibility of arterioles is greater in brain stem than cerebrum, despite greater cross-sectional area of the arteriolar wall in brain stem, and 3) the proportion of elastic components is greater in brain stem than cerebral arterioles, which may contribute to greater arteriolar distensibility in brain stem.