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Journal articles on the topic 'Hemodynamic responses'

Author: Grafiati

Published: 4 June 2021

Last updated: 8 February 2022

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1

Martindale, John, John Mayhew, Jason Berwick, Myles Jones, Chris Martin, Dave Johnston, Peter Redgrave, and Ying Zheng. "The Hemodynamic Impulse Response to a Single Neural Event." Journal of Cerebral Blood Flow & Metabolism 23, no. 5 (May 2003): 546–55. http://dx.doi.org/10.1097/01.wcb.0000058871.46954.2b.

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This article investigates the relation between stimulus-evoked neural activity and cerebral hemodynamics. Specifically, the hypothesis is tested that hemodynamic responses can be modeled as a linear convolution of experimentally obtained measures of neural activity with a suitable hemodynamic impulse response function. To obtain a range of neural and hemodynamic responses, rat whisker pad was stimulated using brief (≤2 seconds) electrical stimuli consisting of single pulses (0.3 millisecond, 1.2 mA) combined both at different frequencies and in a paired-pulse design. Hemodynamic responses were measured using concurrent optical imaging spectroscopy and laser Doppler flowmetry, whereas neural responses were assessed through current source density analysis of multielectrode recordings from a single barrel. General linear modeling was used to deconvolve the hemodynamic impulse response to a single “neural event” from the hemodynamic and neural responses to stimulation. The model provided an excellent fit to the empirical data. The implications of these results for modeling schemes and for physiologic systems coupling neural and hemodynamic activity are discussed.

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2

Premen, A. J. "Splanchnic and renal hemodynamic responses to intraportal infusion of glucagon." American Journal of Physiology-Renal Physiology 253, no. 6 (December 1, 1987): F1105—F1112. http://dx.doi.org/10.1152/ajprenal.1987.253.6.f1105.

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We compared the 60-min splanchnic and renal hemodynamic responses to intraportal (IPV) and intravenous infusion of glucagon (5 ng.kg-1.min-1) in anesthetized dogs and quantitated the importance of glucose in mediating the renal hemodynamic responses to intraportal infusion of glucagon. Intraportal glucagon elevated superior mesenteric (SMA) and renal (RA) artery blood flows by 8 and 16%, respectively, by minute 15. By minute 30, RA flow had increased by 23%. Thereafter, SMA flow returned to control, while RA flow remained elevated by 24%. Glomerular filtration rate (GFR) followed the same pattern as RA flow over 60 min. Intravenous glucagon elicited smaller hemodynamic responses. During intraportal and intravenous glucagon infusion, plasma glucose rose by 20-25%. Renal hemodynamics were not affected by incremental changes in blood glucose of up to 6.25 mmol/l. At an incremental change in glucose of 10.06 mmol/l, RA flow and GFR were elevated by 12 and 9%, respectively. We conclude that intraportal glucagon infusion increases splanchnic and renal hemodynamics, although the splanchnic response is evanescent. Importantly, hepatic release of glucose into the circulation during intraportal glucagon infusion does not have a significant effect on renal hemodynamics. Thus, similar to intravenous infusion of the hormone, renal hemodynamic responses to intraportal glucagon are independent of and dissociated from elevations in blood glucose produced during hormone infusion.

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3

D'souza, Olvyna, and Suman Sahu. "Effect of Dexmedetomidine in Attenuating Hemodynamic Responses During Extubation." Indian Journal of Anesthesia and Analgesia 6, no. 2 (2019): 619–25. http://dx.doi.org/10.21088/ijaa.2349.8471.6219.38.

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4

Jahr, Jonathan S., Bin Kang, Carlos G. Paxtor, and Chang Jian Feng. "HEMODYNAMIC RESPONSES TO PAPAVERINE." American Journal of Therapeutics 2, no. 4 (April 1995): 258–64. http://dx.doi.org/10.1097/00045391-199504000-00007.

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5

Kennerley, Aneurin J., Sam Harris, Michael Bruyns-Haylett, Luke Boorman, Ying Zheng, Myles Jones, and Jason Berwick. "Early and Late Stimulus-Evoked Cortical Hemodynamic Responses Provide Insight into the Neurogenic Nature of Neurovascular Coupling." Journal of Cerebral Blood Flow & Metabolism 32, no. 3 (November 30, 2011): 468–80. http://dx.doi.org/10.1038/jcbfm.2011.163.

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Understanding neurovascular coupling is a prerequisite for the interpretation of results obtained from modern neuroimaging techniques. This study investigated the hemodynamic and neural responses in rat somatosensory cortex elicited by 16 seconds electrical whisker stimuli. Hemodynamics were measured by optical imaging spectroscopy and neural activity by multichannel electrophysiology. Previous studies have suggested that the whisker-evoked hemodynamic response contains two mechanisms, a transient ‘backwards’ dilation of the middle cerebral artery, followed by an increase in blood volume localized to the site of neural activity. To distinguish between the mechanisms responsible for these aspects of the response, we presented whisker stimuli during normocapnia (‘control’), and during a high level of hypercapnia. Hypercapnia was used to ‘predilate’ arteries and thus possibly ‘inhibit’ aspects of the response related to the ‘early’ mechanism. Indeed, hemodynamic data suggested that the transient stimulus-evoked response was absent under hypercapnia. However, evoked neural responses were also altered during hypercapnia and convolution of the neural responses from both the normocapnic and hypercapnic conditions with a canonical impulse response function, suggested that neurovascular coupling was similar in both conditions. Although data did not clearly dissociate early and late vascular responses, they suggest that the neurovascular coupling relationship is neurogenic in origin.

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6

Lefferts, Elizabeth C., Alexander J. Rosenberg, Georgios Grigoriadis, Sang Ouk Wee, Stephen Kerber, Kenneth W. Fent, Gavin P. Horn, Denise L. Smith, and Bo Fernhall. "Firefighter hemodynamic responses to different fire training environments." Vascular Medicine 26, no. 3 (February 19, 2021): 240–46. http://dx.doi.org/10.1177/1358863x20987608.

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Firefighting is associated with an increased risk for a cardiovascular (CV) event, likely due to increased CV strain. The increase in CV strain during firefighting can be attributed to the interaction of several factors such as the strenuous physical demand, sympathetic nervous system activation, increased thermal burden, and the environmental exposure to smoke pollutants. Characterizing the impact of varying thermal burden and pollutant exposure on hemodynamics may help understand the CV burden experienced during firefighting. The purpose of this study was to examine the hemodynamic response of firefighters to training environments created by pallets and straw; oriented strand board (OSB); or simulated fire/smoke (fog). Twenty-three firefighters had brachial blood pressure measured and central blood pressure and hemodynamics estimated from the pressure waveform at baseline, and immediately and 30 minutes after each scenario. The training environment did not influence the hemodynamic response over time (interaction, p > 0.05); however, OSB scenarios resulted in higher pulse wave velocity and blood pressure (environment, p < 0.05). In conclusion, conducting OSB training scenarios appears to create the largest arterial burden in firefighters compared to other scenarios in this study. Environmental thermal burden in combination with the strenuous exercise, and psychological and environmental stress placed on firefighters should be considered when designing fire training scenarios and evaluating CV risk.

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7

Liu, Spencer S., and Randall L. Carpenter. "Hemodynamic Responses to Intravascular Injection of Epinephrine-containing Epidural Test Doses in Adults during General Anesthesia." Anesthesiology 84, no. 1 (January 1, 1996): 81–87. http://dx.doi.org/10.1097/00000542-199601000-00010.

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Background Epidural anesthesia is sometimes initiated during general anesthesia, yet few data exist concerning efficacy of epinephrine-containing test doses. Methods Thirty-six patients were randomized to receive either 0.5 MAC isoflurane, 1 MAC isoflurane, or 0.5 MAC each (1 MAC total) of isoflurane and nitrous oxide. Each subject received intravenous saline followed by three test doses containing 45 mg lidocaine with 7.5, 15, and 30 micrograms epinephrine in a randomized, double-blind fashion. Heart rate and systolic, diastolic, and mean blood pressures were measured for 5 min after injection. Positive hemodynamic criteria identifying intravascular injection were determined from peak increases in hemodynamics during administration of saline. Dose-effect relationships between epinephrine and peak increases in hemodynamics were assessed with linear regression. Minimum required doses of epinephrine to produce peak positive hemodynamic increases on average were determined from linear regression. Results Positive hemodynamic criteria were identified as increases in heart rate > or = 8 beats/min, systolic blood pressure > or = 13 mmHg, diastolic blood pressure > or = 7 mmHg, and mean blood pressure > or = 9 mmHg. Significant dose-effect relationships were observed for epinephrine and peak increases in hemodynamics (correlation coefficients ranged from 0.61-0.91). Minimum required doses of epinephrine ranged from 6 to 19 micrograms depending on hemodynamic measurement and anesthetic group. Conclusions Hemodynamic responses to intravascular injection of test doses vary with dose of epinephrine and depth and type of general anesthetic used. Thus, the 15 micrograms epinephrine contained in the standard test dose may not be sufficient during all anesthetic conditions.

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8

Ohsumi, H., M. Sakamoto, T. Yamazaki, and F. Okumura. "Effects of fentanyl on carotid sinus baroreflex control of circulation in rabbits." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 256, no. 3 (March 1, 1989): R625—R631. http://dx.doi.org/10.1152/ajpregu.1989.256.3.r625.

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The effects of intravenous administration of fentanyl on carotid sinus baroreflex control of hemodynamics were investigated in chronically instrumented rabbits. Carotid sinus baroreflex was assessed by bilateral carotid occlusion (BCO), and the responses of mean arterial pressure (MAP), heart rate (HR), mean ascending aortic flow (MAF), and total peripheral resistance (TPR) were obtained. Hemodynamic responses to BCO were examined with cumulative doses of 5, 10, and 15 micrograms/kg of fentanyl. Fentanyl did not affect MAP and TPR but reduced HR and MAF dose dependently. Fentanyl did not attenuate the MAP response to BCO significantly. In contrast, fentanyl significantly attenuated the TPR response from 0.126 +/- 0.003 to 0.104 +/- 0.005 mmHg.min-1.ml-1 and augmented the HR response from 31 +/- 2 to 47 +/- 3 beats/min in the conscious state and at 15 micrograms/kg of fentanyl, respectively. The administration of atropine after the fentanyl attenuated MAP and HR responses to 79.9 and 27.7% of those of 10 micrograms/kg of fentanyl, respectively. We suggest that these dissociated hemodynamic responses reflect the vagotonic and sympatholytic effects of fentanyl on the baroreflex pathways.

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9

Ford, Judith M., Matthew B. Johnson, Susan L. Whitfield, William O. Faustman, and Daniel H. Mathalon. "Delayed hemodynamic responses in schizophrenia." NeuroImage 26, no. 3 (July 2005): 922–31. http://dx.doi.org/10.1016/j.neuroimage.2005.03.001.

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10

Behnia, Rahim, Colin A. Shanks, Andranik Ovassapian, and Lawrence A. Wilson. "Hemodynamic Responses Associated with Lithotripsy." Anesthesia & Analgesia 66, no. 4 (April 1987): 354???356. http://dx.doi.org/10.1213/00000539-198704000-00014.

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11

Venturelli, Massimo, M. Amann, J. McDaniel, J. D. Trinity, A. S. Fjeldstad, and R. S. Richardson. "Central and peripheral hemodynamic responses to passive limb movement: the role of arousal." American Journal of Physiology-Heart and Circulatory Physiology 302, no. 1 (January 2012): H333—H339. http://dx.doi.org/10.1152/ajpheart.00851.2011.

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The exact role of arousal in central and peripheral hemodynamic responses to passive limb movement in humans is unclear but has been proposed as a potential contributor. Thus, we used a human model with no lower limb afferent feedback to determine the role of arousal on the hemodynamic response to passive leg movement. In nine people with a spinal cord injury, we compared central and peripheral hemodynamic and ventilatory responses to one-leg passive knee extension with and without visual feedback (M+VF and M-VF, respectively) as well as in a third trial with no movement or visual feedback but the perception of movement (F). Ventilation (V̇e), heart rate, stroke volume, cardiac output, mean arterial pressure, and leg blood flow (LBF) were evaluated during the three protocols. V̇e increased rapidly from baseline in M+VF (55 ± 11%), M-VF (63 ± 13%), and F (48 ± 12%) trials. Central hemodynamics (heart rate, stroke volume, cardiac output, and mean arterial pressure) were unchanged in all trials. LBF increased from baseline by 126 ± 18 ml/min in the M+VF protocol and 109 ± 23 ml/min in the M-VF protocol but was unchanged in the F protocol. Therefore, with the use of model that is devoid of afferent feedback from the legs, the results of this study reveal that, although arousal is invoked by passive movement or the thought of passive movement, as evidenced by the increase in V̇e, there is no central or peripheral hemodynamic impact of this increased neural activity. Additionally, this study revealed that a central hemodynamic response is not an obligatory component of movement-induced LBF.

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12

Venturelli, Massimo, Susanna Rampichini, Giuseppe Coratella, Eloisa Limonta, Angela Valentina Bisconti, Emiliano Cè, and Fabio Esposito. "Heart and musculoskeletal hemodynamic responses to repetitive bouts of quadriceps static stretching." Journal of Applied Physiology 127, no. 2 (August 1, 2019): 376–84. http://dx.doi.org/10.1152/japplphysiol.00823.2018.

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The role of sympathetic and parasympathetic activity in relation to the repetitive exposure to static stretching (SS) on heart and musculoskeletal hemodynamics in stretched and resting muscles is still a matter of debate. The aim of the study was to determine cardiac and musculoskeletal hemodynamics to repetitive bouts of unilateral SS. Sympathetic and parasympathetic activity contribution to the central hemodynamics and local difference in circulation of stretched and resting muscles were also investigated. In eight participants, heart rate (HR), cardiac output (CO), mean arterial pressure (MAP), HR variability (HRV), blood pressure variability (BPV), and blood flow in passively stretched limb (SL) and control (CL, resting limb) were measured during five bouts of unilateral SS (45 s of knee flexion and 15 s of knee extension). SS increased sympathetic (~20%) and decreased parasympathetic activity (~30%) with a prevalence of parasympathetic withdrawal. During SS, HR, CO, and MAP increased by ~18 beats/min, ~0.29 l/min, ~12 mmHg, respectively. Peak blood flow in response to the first stretching maneuver increased significantly (+377 ± 95 ml/min) in the SL and reduced significantly (−57 ± 48 ml/min) in the CL. This between-limb difference in local circulation response to SS disappeared after the second SS bout. These results indicate that heart hemodynamic responses to SS are primarily influenced by the parasympathetic withdrawal rather than by the increase in sympathetic activity. The balance between neural and local factors contributing to blood flow regulation was affected by the level of SS exposure, likely associated with differences in the bioavailability of local vasoactive factors throughout the stretching bouts. NEW & NOTEWORTHY Repetitive exposure to static stretching (SS) on heart and musculoskeletal hemodynamics in stretched and remote muscles may be influenced by neural and local factors. We documented that SS-induced heart hemodynamic responses are primarily influenced by parasympathetic withdrawal. The balance between neural and local factors contributing to the regulation of musculoskeletal hemodynamics is dependent on SS exposure possibly because of different local vasoactive factor bioavailability during the subsequent stretching bouts.

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13

Berwick, J., D. Johnston, M. Jones, J. Martindale, C. Martin, A. J. Kennerley, P. Redgrave, and J. E. W. Mayhew. "Fine Detail of Neurovascular Coupling Revealed by Spatiotemporal Analysis of the Hemodynamic Response to Single Whisker Stimulation in Rat Barrel Cortex." Journal of Neurophysiology 99, no. 2 (February 2008): 787–98. http://dx.doi.org/10.1152/jn.00658.2007.

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The spatial resolution of hemodynamic-based neuroimaging techniques, including functional magnetic resonance imaging, is limited by the degree to which neurons regulate their blood supply on a fine scale. Here we investigated the spatial detail of neurovascular events with a combination of high spatiotemporal resolution two-dimensional spectroscopic optical imaging, multichannel electrode recordings and cytochrome oxidase histology in the rodent whisker barrel field. After mechanical stimulation of a single whisker, we found two spatially distinct cortical hemodynamic responses: a transient response in the “upstream” branches of surface arteries and a later highly localized increase in blood volume centered on the activated cortical column. Although the spatial representation of this localized response exceeded that of a single “barrel,” the spread of hemodynamic activity accurately reflected the neural response in neighboring columns rather than being due to a passive “overspill.” These data confirm hemodynamics are capable of providing accurate “single-condition” maps of neural activity.

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14

Goetz, K. L., B. C. Wang, P. G. Geer, W. D. Sundet, and P. Needleman. "Effects of atriopeptin infusion versus effects of left atrial stretch in awake dogs." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 250, no. 2 (February 1, 1986): R221—R226. http://dx.doi.org/10.1152/ajpregu.1986.250.2.r221.

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We infused synthetic atriopeptin III intravenously into 10 conscious dogs while monitoring renal function and systemic hemodynamics. The results obtained from these infusion experiments were compared with results from other experiments in which left atrial distension was performed in the same dogs. Both atriopeptin infusion and left atrial distension caused significant increases in urine flow, sodium excretion, potassium excretion, and free water reabsorption and a significant decrease in renal blood flow. On the other hand, the pattern of systemic hemodynamic responses to atriopeptin infusion were quite different from the hemodynamic responses elicited by left atrial distension. However, there was a striking concordance between the renal effects of atriopeptin and those of left atrial distension. We therefore hypothesize that the renal response to left atrial distension in the conscious dog is mediated largely by the release of natriuretic peptides from the atria.

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15

Crystal, G. J. "Coronary hemodynamic responses during local hemodilution in canine hearts." American Journal of Physiology-Heart and Circulatory Physiology 254, no. 3 (March 1, 1988): H525—H531. http://dx.doi.org/10.1152/ajpheart.1988.254.3.h525.

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To evaluate the effect of hemodilution per se on coronary hemodynamics, experiments were performed in 36 anesthetized, open-chest dogs whose left anterior descending coronary artery (LAD) was perfused selectively with either normal arterial blood or arterial blood diluted with lactated Ringer solution. LAD blood flow (CBF) was measured with an electromagnetic flowmeter and its transmural distribution assessed with 15-microns radioactive microspheres. LAD perfusion pressure was set at the normal level (approximately 100 mmHg) or at 50% of that level to simulate coronary insufficiency. Dilator reserve capacity was calculated from ratio of reactive hyperemic peak flow following release of 90-s occlusion to control (preocclusion) flow. Systemic hemodynamic parameters were maintained near control values during coronary hemodilution. With perfusion pressure normal, graded hemodilution caused progressive, transmurally uniform increases in CBF that showed a nonlinear relationship to inflow hematocrit. Increased peak reactive hyperemic flow and decreased dilator reserve ratio indicated that both reduced viscosity and vasodilation contributed to increased CBF during hemodilution. Hypotension alone reduced CBF, with greater effect in the subendocardium. Additional hemodilution returned CBF to normotensive value, but relative subendocardial hypoperfusion persisted. The present study provides fundamental information on effects of hemodilution on coronary hemodynamics without the systemic responses that complicated previous studies utilizing whole body exchange transfusions.

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16

JENSENURSTAD, M., B. BERGLUND, F. BOUVIER, L. JORFELDT, A. JUHLINDANNFELT, M. NEJAT, B. SALTIN, and L. BRODIN. "Hemodynamic responses to exercise in runners." Journal of Nuclear Cardiology 2, no. 2 (March 1995): S102. http://dx.doi.org/10.1016/s1071-3581(05)80493-3.

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17

Brown, S. P., H. Li, L. F. Chitwood, E. R. Anderson, and J. D. Boatwright. "489 RECOVERY THERMAL AND HEMODYNAMIC RESPONSES." Medicine & Science in Sports & Exercise 25, Supplement (May 1993): S86. http://dx.doi.org/10.1249/00005768-199305001-00491.

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18

Fujimoto, Naoki, Barry A. Borlaug, Gregory D. Lewis, Jeffrey L. Hastings, Keri M. Shafer, Paul S. Bhella, Graeme Carrick-Ranson, and Benjamin D. Levine. "Hemodynamic Responses to Rapid Saline Loading." Circulation 127, no. 1 (January 2013): 55–62. http://dx.doi.org/10.1161/circulationaha.112.111302.

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19

Grasser, Erik Konrad, Jennifer Lynn Miles-Chan, and Jean-Pierre Montani. "Hemodynamic Responses to Energy Drink Consumption." JAMA 315, no. 18 (May 10, 2016): 2018. http://dx.doi.org/10.1001/jama.2016.1109.

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20

Minkes, Robert K., and Philip J. Kadowitz. "Hemodynamic Responses to Sarafotoxin 6 Peptides." Journal of Cardiovascular Pharmacology 17 (1991): S293–296. http://dx.doi.org/10.1097/00005344-199100177-00083.

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21

Brassard, Patrice, and Paul Poirier. "Diabetes and exercise-induced hemodynamic responses." Diabetes Research and Clinical Practice 78, no. 1 (October 2007): 147–48. http://dx.doi.org/10.1016/j.diabres.2007.03.003.

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22

Hung, Orlando. "Understanding hemodynamic responses to tracheal intubation." Canadian Journal of Anesthesia/Journal canadien d'anesthésie 48, no. 8 (September 2001): 723–26. http://dx.doi.org/10.1007/bf03016684.

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23

Tang, C. S., H. Cui, Q. X. Yuan, and J. Tang. "Hemodynamic responses to BNP in rats." European Journal of Pharmacology 159, no. 3 (January 1989): 327–28. http://dx.doi.org/10.1016/0014-2999(89)90168-4.

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24

Wilund, Ken, Jinhee Jeong, Bo Fernhall, Annabel Biruete, Luis Perez, and Kersten Mitchell. "MP467ACUTE HEMODYNAMIC RESPONSES TO INTRADIALYTIC EXERCISE." Nephrology Dialysis Transplantation 32, suppl_3 (May 1, 2017): iii600. http://dx.doi.org/10.1093/ndt/gfx173.mp467.

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25

Makwama, D. S., J. M. Thakkar, R. Majmudar, A. Shnodhi, G. Malviya, and B. M. Patel. "Clonidine Premedication Decreases Hemodynamic Responses to Pin Head-Holder Application during Craniotomy." Asian Pacific Journal of Health Sciences 2, no. 3 (July 2015): 57–61. http://dx.doi.org/10.21276/apjhs.2015.2.3.13.

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26

Brix, Bianca, Olivier White, Christian Ure, Gert Apich, Paul Simon, Andreas Roessler, and Nandu Goswami. "Hemodynamic Responses in Lower Limb Lymphedema Patients Undergoing Physical Therapy." Biology 10, no. 7 (July 10, 2021): 642. http://dx.doi.org/10.3390/biology10070642.

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Background: Lymphedema arises due to a malfunction of the lymphatic system, leading to extensive tissue swelling. Complete decongestive therapy (CDT), which is a physical therapy lasting for 3 weeks and includes manual lymphatic drainages (MLD), leads to fluid mobilization and increases in plasma volume. Here, we investigated hemodynamic responses induced by these fluid shifts due to CDT and MLD. Methods: Hemodynamic parameters were assessed continuously during a sit-to-stand test (5 min baseline, 5 min of standing, and 5 min of recovery). This intervention was repeated on days 1, 2, 7, 14, and 21 of CDT, before and after MLD. Volume regulatory hormones were assessed in plasma samples. Results: A total number of 13 patients took part in this investigation. Resting diastolic blood pressure significantly decreased over three weeks of CDT (p = 0.048). No changes in baseline values were shown due to MLD. However, MLD led to a significant decrease in heart rate during orthostatic loading over all epochs on therapy day 14, as well as day 21. Volume regulatory hormones did not show changes over lymphedema therapy. Conclusion: We did not observe any signs of orthostatic hypotension at rest, as well as during to CDT, indicating that lymphedema patients do not display an elevated risk of orthostatic intolerance. Although baseline hemodynamics were not affected, MLD has shown to have potential beneficial effects on hemodynamic responses to a sit-to-stand test in patients undergoing lymphedema therapy.

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27

Tucker, B. J., O. W. Peterson, K. A. Munger, J. E. Bird, M. Mitchell, J. C. Pelayo, and R. C. Blantz. "Glomerular hemodynamic alterations during renal nerve stimulation in rats on high- and low-salt diets." American Journal of Physiology-Renal Physiology 258, no. 1 (January 1, 1990): F133—F143. http://dx.doi.org/10.1152/ajprenal.1990.258.1.f133.

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Renal adrenergic nerve activity exerts a major influence on glomerular hemodynamics and tubular fluid reabsorption. Modulation of the functional expression of adrenergic activity in the kidney can be mediated, in part, by the renin-angiotensin system and by prostanoid activity. Alterations in dietary salt intake have been previously shown to modify the activity of various vasoactive systems, including angiotensin and prostaglandin activity and thereby have a potential of modifying the glomerular hemodynamic response to a given renal adrenergic stimulus. Munich-Wistar rats were fed either a high-, low-, or normal salt diet for 2 wk before the day of the study. Measurements of glomerular hemodynamics were performed in both unstimulated with basal renal nerve traffic eliminated and during exogenous renal nerve stimulation (RNS) (3 Hz). RNS decreased glomerular capillary hydrostatic pressure and single-nephron plasma flow to a similar extent in all three dietary conditions via increases in afferent arteriolar resistance. The data demonstrated that dietary preconditioning does not alter the glomerular hemodynamic response to an exogenous, fixed RNS. Glomerular prostaglandin E2 production and plasma renin activity were significantly greater in rats fed a low-salt diet compared with either normal- or high-salt diet. The constancy of glomerular hemodynamic responses to RNS in spite of wide variations in dietary salt intake indicates that functional renal hemodynamic differences observed as a result of NaCl intake must be primarily the consequence of differences in renal nerve traffic and not hormonal alterations.

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28

Frazier, Susan K., Kathleen S. Stone, Eric R. Schertel, Debra K. Moser, and Jerry W. Pratt. "A Comparison of Hemodynamic Changes during the Transition from Mechanical Ventilation to T-Piece, Pressure Support, and Continuous Positive Airway Pressure in Canines." Biological Research For Nursing 1, no. 4 (April 2000): 253–64. http://dx.doi.org/10.1177/109980040000100402.

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The immediate transition from positive pressure mechanical ventilation to spontaneous ventilation may generate significant cardiopulmonary hemodynamic alterations based on the mode of weaning selected, particularly in individuals with preexisting cardiac dysfunction. The purpose of this study was to compare hemodynamic responses associated with the initial transition to 3 modes of ventilator weaning (spontaneous ventilation/T-piece, pressure support [PS], and continuous positive airway pressure [CPAP]). Right ventricular hemodynamic responses were evaluated with a thermodilution pulmonary artery catheter; while left ventricular hemodynamic responses were measured by a transducer-tipped Millar catheter and conductance catheter. Two groups of canines were studied. Group 1: normal biventricular function (n = 10) and group 2: propranolol-induced biventricular failure (n = 10). Dependent variables were measured at baseline on controlled mechanical ventilation (MV) and following the initial transition to each of 3 randomized spontaneous ventilatory conditions: T-piece, PS 5 cmH2O, and CPAP 5 cmH2O. Both groups significantly increased cardiac output in response to T-piece. Right ventricular stroke work was also significantly increased with T-piece and CPAP in both groups of subjects. Left ventricular response depended on baseline ventricular function. Baseline ventricular function influenced hemodynamic response to the immediate transition from mechanical to spontaneous ventilation. There were also differential hemodynamic responses based on the ventilatory mode. Consideration of baseline cardiac function may be an important factor in the selection of an appropriate mode of spontaneous ventilation following controlled MV.

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29

Mulheren, Rachel W., Erin Kamarunas, and Christy L. Ludlow. "Sour taste increases swallowing and prolongs hemodynamic responses in the cortical swallowing network." Journal of Neurophysiology 116, no. 5 (November 1, 2016): 2033–42. http://dx.doi.org/10.1152/jn.00130.2016.

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Sour stimuli have been shown to upregulate swallowing in patients and in healthy volunteers. However, such changes may be dependent on taste-induced increases in salivary flow. Other mechanisms include genetic taster status (Bartoshuk LM, Duffy VB, Green BG, Hoffman HJ, Ko CW, Lucchina LA, Weiffenbach JM. Physiol Behav 82: 109–114, 2004) and differences between sour and other tastes. We investigated the effects of taste on swallowing frequency and cortical activation in the swallowing network and whether taster status affected responses. Three-milliliter boluses of sour, sour with slow infusion, sweet, water, and water with infusion were compared on swallowing frequency and hemodynamic responses. The sour conditions increased swallowing frequency, whereas sweet and water did not. Changes in cortical oxygenated hemoglobin (hemodynamic responses) measured by functional near-infrared spectroscopy were averaged over 30 trials for each condition per participant in the right and left motor cortex, S1 and supplementary motor area for 30 s following bolus onset. Motion artifact in the hemodynamic response occurred 0–2 s after bolus onset, when the majority of swallows occurred. The peak hemodynamic response 2–7 s after bolus onset did not differ by taste, hemisphere, or cortical location. The mean hemodynamic response 17–22 s after bolus onset was highest in the motor regions of both hemispheres, and greater in the sour and infusion condition than in the water condition. Genetic taster status did not alter changes in swallowing frequency or hemodynamic response. As sour taste significantly increased swallowing and cortical activation equally with and without slow infusion, increases in the cortical swallowing were due to sour taste.

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Nakata, Yoshinori, Takahisa Goto, Hayato Saito, Yoshiki Ishiguro, Katsuo Terui, Hiromasa Kawakami, Yoshihiko Tsuruta, Yoshinari Niimi, and Shigeho Morita. "Plasma Concentration of Fentanyl with Xenon to Block Somatic and Hemodynamic Responses to Surgical Incision." Anesthesiology 92, no. 4 (April 1, 2000): 1043–48. http://dx.doi.org/10.1097/00000542-200004000-00022.

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Background Although anesthesia with xenon has been supplemented with fentanyl, its requirement has not been established. This study was conducted to determine the plasma concentrations of fentanyl necessary to suppress somatic and hemodynamic responses to surgical incision in 50% patients in the presence of 0.7 minimum alveolar concentration (MAC) xenon. Methods Twenty-five patients were allocated randomly to predetermined fentanyl concentration between 0.5 and 4.0 ng/ml during 0.7 MAC xenon anesthesia. Fentanyl was administered using a pharmacokinetic model-driven computer-assisted continuous infusion device. At surgical incision each patient was monitored for somatic and hemodynamic responses. A somatic response was defined as any purposeful bodily movement. A positive hemodynamic response was defined as a more than 15% increase in heart rate or mean arterial pressure more than the preincision value. The concentrations of fentanyl to prevent somatic and hemodynamic responses in 50% of patients were calculated using logistic regression. Results The concentration of fentanyl to prevent a somatic response to skin incision in 50% of patients in the presence of 0.7 MAC xenon was 0.72 +/- 0.07 ng/ml and to prevent a hemodynamic response was 0.94 +/- 0.06 ng/ml. Conclusions Comparing these results with previously published results in the presence of 70% nitrous oxide, the fentanyl requirement in xenon anesthesia is smaller than that in the equianesthetic nitrous oxide anesthesia.

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Anenberg, Eitan, Allen W. Chan, Yicheng Xie, Jeffrey M. LeDue, and Timothy H. Murphy. "Optogenetic Stimulation of GABA Neurons can Decrease Local Neuronal Activity While Increasing Cortical Blood Flow." Journal of Cerebral Blood Flow & Metabolism 35, no. 10 (June 17, 2015): 1579–86. http://dx.doi.org/10.1038/jcbfm.2015.140.

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We investigated the link between direct activation of inhibitory neurons, local neuronal activity, and hemodynamics. Direct optogenetic cortical stimulation in the sensorimotor cortex of transgenic mice expressing Channelrhodopsin-2 in GABAergic neurons (VGAT-ChR2) greatly attenuated spontaneous cortical spikes, but was sufficient to increase blood flow as measured with laser speckle contrast imaging. To determine whether the observed optogenetically evoked gamma aminobutyric acid (GABA)-neuron hemodynamic responses were dependent on ionotropic glutamatergic or GABAergic synaptic mechanisms, we paired optogenetic stimulation with application of antagonists to the cortex. Incubation of glutamatergic antagonists directly on the cortex (NBQX and MK-801) blocked cortical sensory evoked responses (as measured with electroencephalography and intrinsic optical signal imaging), but did not significantly attenuate optogenetically evoked hemodynamic responses. Significant light-evoked hemodynamic responses were still present after the addition of picrotoxin (GABA-A receptor antagonist) in the presence of the glutamatergic synaptic blockade. This activation of cortical inhibitory interneurons can mediate large changes in blood flow in a manner that is by and large not dependent on ionotropic glutamatergic or GABAergic synaptic transmission. This supports the hypothesis that activation of inhibitory neurons can increase local cerebral blood flow in a manner that is not entirely dependent on levels of net ongoing neuronal activity.

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Milone, Stephen D., Gary E. Newton, and John D. Parker. "Hemodynamic and biochemical effects of 100% oxygen breathing in humans." Canadian Journal of Physiology and Pharmacology 77, no. 2 (February 1, 1999): 124–30. http://dx.doi.org/10.1139/y99-010.

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High concentrations of inspired oxygen have been reported to have significant hemodynamic effects that may be related to increased free radical production. If oxygen therapy increases free radical production, it may also modify hemodynamic responses to a nitric oxide donor. Twenty-nine healthy male volunteers were studied using randomized, double-blind, placebo-controlled, crossover designs to determine whether oxygen therapy is associated with hemodynamic and forearm vascular effects. We measured hemodynamic parameters and forearm vascular responses before and 1 h after exposure to 100% oxygen versus medical air. Plasma 8-iso-PGF2α and plasma vitamin C were measured to assess the biochemical effects of oxygen administration. Hemodynamic measurements were also made following the acute administration of sublingual nitroglycerin. Oxygen therapy caused no significant change in blood pressure, plasma 8-iso-PGF2α, or vitamin C. Oxygen did cause a significant reduction in heart rate and forearm blood flow, and an increase in peripheral vascular resistance. Oxygen caused no change in the hemodynamic response to nitroglycerin. Therefore, in healthy young adults, therapy with 100% oxygen does not affect blood pressure, despite causing an increase in vascular resistance, is not associated with evidence of increased free radical injury, and does not affect the hemodynamic responses to nitroglycerin.Key words: oxygen, nitroglycerin, free radicals, blood pressure, heart rate, plethysmography.

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Cherney, David Z. I., Heather N. Reich, Judith A. Miller, Vesta Lai, Bernard Zinman, Maria G. Dekker, Timothy J. Bradley, James W. Scholey, and Etienne B. Sochett. "Age is a determinant of acute hemodynamic responses to hyperglycemia and angiotensin II in humans with uncomplicated type 1 diabetes mellitus." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 299, no. 1 (July 2010): R206—R214. http://dx.doi.org/10.1152/ajpregu.00027.2010.

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Hyperglycemia is associated with hemodynamic changes in type 1 diabetes (DM), acting in part through renin-angiotensin system activation. Since aging is associated with vascular dysfunction in DM, we hypothesized that acute hemodynamic responses to clamped hyperglycemia and infused ANG II would be exaggerated in older adults compared with a group of adolescent/young adults with type 1 DM. Renal hemodynamic function, blood pressure, and arterial stiffness were assessed in adolescent/young adults ( n = 34; mean age: 18 ± 3 yr) and older adults ( n = 32; mean age: 45 ± 9 yr). Studies were performed during clamped euglycemia (4–6 mmol/l) and hyperglycemia (9–11 mmol/l). Renal and systemic hemodynamic responses to ANG II were measured during clamped euglycemia in diabetic subjects. ANG II responses were also assessed in a cohort of non-DM subjects ( n = 97; mean age: 26; age range: 18–40 yr). Older DM adults exhibited higher baseline blood pressure, arterial stiffness, and renal vascular resistance, and lower glomerular filtration rate (GFR) and effective renal plasma flow, compared with adolescent/young DM adults ( P < 0.05). Clamped hyperglycemia was associated with exaggerated peripheral and renal hemodynamic responses uniquely in older DM adults; only GFR increased in adolescent/young DM adults. ANG II infusion also produced exaggerated vasoconstrictive responses in older DM adults vs. adolescent/young DM adults ( P < 0.05). The independent effect of age on hemodynamic responses to hyperglycemia and ANG II was confirmed using multivariate regression analysis in DM subjects ( P < 0.05), and results were still significant when participants were matched for DM duration. Age-related alterations in hemodynamic function and ANG II response were not observed in healthy non-DM control subjects. Acute hemodynamic responses to clamped hyperglycemia and ANG II were exaggerated in older subjects with type 1 DM, highlighting an important interaction between age and factors that contribute to the pathogenesis of acute vascular dysfunction in DM.

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Brizzee, B. L., L. Harrison-Bernard, H. A. Pretus, G. G. Clifton, and B. R. Walker. "Hemodynamic responses to vasopressinergic antagonism in water-deprived conscious rats." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 255, no. 1 (July 1, 1988): R46—R51. http://dx.doi.org/10.1152/ajpregu.1988.255.1.r46.

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Experiments were performed on conscious, chronically instrumented rats to determine the role of arginine vasopressin (AVP) on the systemic and regional hemodynamic effects of 48-h water deprivation. Arterial and venous catheters as well as pulsed Doppler flow probes were implanted in rats to measure cardiac output (CO), mesenteric blood flow (MBF), renal blood flow (RBF), or hindquarter blood flow (HQBF). After adequate recovery from surgey, euhydrated animals were administered a specific V1-vasopressinergic antagonist [d(CH2)5Tyr(Me)AVP, 10 micrograms/kg iv], a combined V1, V2-antagonist [d(CH2)5DTyr(Et)VAVP, 30 micrograms/kg iv], or saline vehicle (100 microliter/100 g). Neither antagonist was associated with any change in mean arterial blood pressure (MABP), heart rate (HR), systemic or regional flow or vascular resistance. All animals were subsequently water deprived for 48 h, at which time the experiments were repeated. Dehydration was associated with an increase in plasma AVP levels, hematocrit, and MABP but with a decrease in HR. Administration of either the combined V1, V2-antagonist or vehicle had no effect on any systemic or regional hemodynamic variables measured after 48-h dehydration. In contrast, although MABP, CO, MBF, and RBF were unaffected, V1-antagonism resulted in elevated HR, increased HQBF, and decreased hindquarter vascular resistance. In conclusion, AVP does not have a major effect on systemic hemodynamics in the dehydrated rat. However, certain beds may be affected by the relatively moderate levels of plasma AVP elicited during dehydration.

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Massett, Michael P., Stephen J. Lewis, and Kevin C. Kregel. "Effect of heating on the hemodynamic responses to vasoactive agents." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 275, no. 3 (September 1, 1998): R844—R853. http://dx.doi.org/10.1152/ajpregu.1998.275.3.r844.

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During hyperthermia, vasoconstrictor tone in the viscera is lost despite high levels of sympathetic neural outflow and plasma catecholamines, suggesting that vascular responsiveness to adrenergic receptor stimulation is reduced. The purpose of this study was to determine whether adrenoceptor-mediated control of vascular resistance is altered at high body core temperatures. The hemodynamic responses to adrenoceptor agonists were examined in chloralose-anesthetized rats heated to colonic temperatures (Tco) of 37, 39, and 41.5°C. Elevating Tco to 39°C did not alter the hemodynamic responses to any of these agents. Further heating to 41.5°C markedly attenuated the hemodynamic responses to α- and β-adrenoceptor agonists. Similarly, the regional and systemic hemodynamic responses to ANG II and endothelin were also reduced at 41.5°C. In contrast, the hemodynamic responses to endothelium-dependent and -independent vasodilator agents were unchanged or slightly reduced at 41.5°C. The blunted hemodynamic responses observed at 41.5°C indicate that vascular reactivity to vasoconstrictor agents is reduced with hyperthermia and suggest that this nonspecific change in vascular responsiveness may contribute the circulatory collapse associated with high body temperatures.

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Obayashi, K., R. Hörnsten, U. Wiklund, M. Karlsson, S. Okamoto, Y. Ando, and O. B. Suhr. "Hemodynamic responses after tilt reversal in FAP." Amyloid 18, sup1 (June 2011): 166–68. http://dx.doi.org/10.3109/13506129.2011.574354062.

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Schneider, Stefan, Vanja Sebastian Zander, Tobias Vogt, Vera Abeln, Heiko K. Strüder, Amrei Jacubowski, Heather Carnahan, and Petra Wollseiffen. "Hemodynamic and Neuroendocrinological Responses to Artificial Gravity." Gravitational and Space Research 5, no. 2 (July 21, 2020): 80–88. http://dx.doi.org/10.2478/gsr-2017-0012.

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AbstractThe aim of this study was to determine the hemodynamic and neuroendocrinological responses to different levels and protocols of artificial gravity, especially in comparison to what is expected during a moderate bout of exercise. Ten male participants were exposed to artificial gravity using two different protocols: the first was a centrifugation protocol that consisted of a constant phase of 2 Gz for 30 minutes, and the second consisted of an intermittent phase of 2 Gz for two minutes, separated by resting periods for three minutes in successive order. Near infrared spectroscopy (oxyhemoglobin and deoxyhemoglobin) at the prefrontal cortex, Musculus biceps brachii, and Musculus gastrocnemius, as well as heart rate and blood pressure were recorded before, during, and after exposure to artificial gravity. In order to determine effects of artificial gravity on neuroendocrinological parameters (brain-derived neurotrophic factor, vascular endothelial growth factor, and insulin-like growth factor 1), blood samples were taken before and after centrifugation. During the application of artificial gravity the concentration of oxyhemoglobin decreased significantly and the concentration of deoxyhemoglobin increased significantly in the prefrontal cortex and the Musculus biceps brachii muscle. Participants exposed to the continuous artificial gravity profile experienced peripheral pooling of blood. No changes were observed for brain-derived neurotrophic factor, vascular endothelial growth factor, or insulin-like growth factor 1. Intermittent application of artificial gravity may represent a better-tolerated presentation for participants as hemodynamic values normalize during resting periods. During both protocols, heart rate and arterial blood pressure remained far below what is experienced during moderate physical activity.

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Lemen, L. C., P. T. Fox, M. G. Woldorff, S. McGinnis, P. A. Jerabek, and J.-H. Gao. "Sustained Visual Stimulation: Neuronal And Hemodynamic Responses." NeuroImage 7, no. 4 (May 1998): S263. http://dx.doi.org/10.1016/s1053-8119(18)31096-6.

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Aguirre, GK, E. Zarahn, and M. D’Esposito. "The variability of human BOLD hemodynamic responses." NeuroImage 7, no. 4 (May 1998): S574. http://dx.doi.org/10.1016/s1053-8119(18)31407-1.

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Stefanovic, Bojana, Jan M. Warnking, and G. Bruce Pike. "Hemodynamic and metabolic responses to neuronal inhibition." NeuroImage 22, no. 2 (June 2004): 771–78. http://dx.doi.org/10.1016/j.neuroimage.2004.01.036.

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41

Alton, Sheila M. "Hemodynamic responses to penetrating spinal cord injuries." Annals of Emergency Medicine 23, no. 3 (March 1994): 639. http://dx.doi.org/10.1016/s0196-0644(94)80402-8.

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Vincent, Kevin R., Heather K. Vincent, Randy W. Braith, Vineesh Bhatnagar, and David T. Lowenthal. "Strength Training and Hemodynamic Responses to Exercise." American Journal of Geriatric Cardiology 12, no. 2 (March 2003): 97–106. http://dx.doi.org/10.1111/j.1076-7460.2003.01588.x.

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43

Hoshi, Yoko, Shunji Kohri, Yoshinori Matsumoto, Kazutoshi Cho, Tadashi Matsuda, Satoru Okajima, and Seiichiro Fujimoto. "Hemodynamic responses to photic stimulation in neonates." Pediatric Neurology 23, no. 4 (October 2000): 323–27. http://dx.doi.org/10.1016/s0887-8994(00)00195-8.

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Mookerjee, Swapan, Ansgar Steegmans, Uwe Drescher, Axel Knicker, and Uwe Hoffmann. "Hemodynamic Responses Following High Intensity Isokinetic Exercise." Medicine & Science in Sports & Exercise 42 (October 2010): 79–80. http://dx.doi.org/10.1249/01.mss.0000389412.11569.25.

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45

Zipnick, Richard I., Thomas M. Scalea, Stanley Z. Trooskin, Salvatore J. A. Sclafani, Behzad Emad, Alpesh Shah, Susan Talbert, and Thomas Haher. "HEMODYNAMIC RESPONSES TO PENETRATING SPINAL CORD INJURIES." Journal of Trauma: Injury, Infection, and Critical Care 35, no. 4 (October 1993): 578–83. http://dx.doi.org/10.1097/00005373-199310000-00013.

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Karlsdottir, Arna E., Carl Foster, John P. Porcari, Karen Palmer-McLean, Roseanne White-Kube, and Richard C. Backes. "Hemodynamic Responses During Aerobic and Resistance Exercise." Journal of Cardiopulmonary Rehabilitation 22, no. 3 (May 2002): 170–77. http://dx.doi.org/10.1097/00008483-200205000-00008.

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47

Doñamayor, Nuria, Urs Heilbronner, and Thomas F. Münte. "Coupling electrophysiological and hemodynamic responses to errors." Human Brain Mapping 33, no. 7 (May 26, 2011): 1621–33. http://dx.doi.org/10.1002/hbm.21305.

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Lathers, C. M., J. B. Charles, K. F. Elton, T. A. Holt, C. Mukai, B. S. Bennett, and M. W. Bungo. "Acute Hemodynamic Responses to Weightlessness in Humans." Journal of Clinical Pharmacology 29, no. 7 (July 1989): 615–27. http://dx.doi.org/10.1002/j.1552-4604.1989.tb03390.x.

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Svatikova, Anna, Naima Covassin, and Kiran R. Somers. "Hemodynamic Responses to Energy Drink Consumption—Reply." JAMA 315, no. 18 (May 10, 2016): 2018. http://dx.doi.org/10.1001/jama.2016.1115.

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SEBEL, PETER S., JOHN F. HOKE, CHERYL WESTMORELAND, CARL C. HUG, KEITH T. MUIR, and FANIA SZLAM. "Histamine Concentrations and Hemodynamic Responses After Remifentanil." Survey of Anesthesiology 40, no. 1 (February 1996): 32. http://dx.doi.org/10.1097/00132586-199602000-00033.

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