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Relevant bibliographies by topics / Depressed vasomotor tone

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Journal articles

Academic literature on the topic 'Depressed vasomotor tone'

Author: Grafiati

Published: 3 June 2025

Last updated: 31 July 2025

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Journal articles on the topic "Depressed vasomotor tone"

1

Poon, Yan-Yuen, Yueh-Wei Liu, Ya-Hui Huang, Samuel H. H. Chan, and Ching-Yi Tsai. "Postoperative Stroke after Spinal Anesthesia and Responses of Carotid or Cerebral Blood Flow and Baroreflex Functionality to Spinal Bupivacaine in Rats." Biology 10, no. 7 (2021): 617. http://dx.doi.org/10.3390/biology10070617.

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Spinal anesthesia is generally accepted as an effective and safe practice. Three rare incidents of postoperative cerebral infarction after surgery under spinal anesthesia prompted us to assess whether spinal bupivacaine may compromise carotid or cerebral blood flow. Postoperative examination after the stroke incident revealed that all three patients shared a common pathology of stenosis or atheromatosis in the carotid or middle cerebral artery. In a companion study using 69 Sprague-Dawley rats, subarachnoid application of bupivacaine elicited an initial (Phase I) reduction in the mean arterial

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2

Sinkler, Shenghua Y., and Steven S. Segal. "Aging alters reactivity of microvascular resistance networks in mouse gluteus maximus muscle." American Journal of Physiology-Heart and Circulatory Physiology 307, no. 6 (2014): H830—H839. http://dx.doi.org/10.1152/ajpheart.00368.2014.

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Aging occurs with enhanced sympathetic nerve activity and endothelial dysfunction; however, little is known of how successive branches of microvascular resistance networks are affected in vivo. We questioned whether vascular reactivity is altered differentially along resistance networks with advanced age. The left gluteus maximus muscle of anesthetized 4-mo-old and 24-mo-old male C57BL/6 mice (Young and Old, respectively) was exposed for intravital microscopy and superfused with physiological salt solution (3 ml/min; pH 7.4, 34°C). Spontaneous vasomotor tone increased progressively from proxim

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3

Olver, T. Dylan, Zachary I. Grunewald, Thaysa Ghiarone, et al. "Persistent insulin signaling coupled with restricted PI3K activation causes insulin-induced vasoconstriction." American Journal of Physiology-Heart and Circulatory Physiology 317, no. 5 (2019): H1166—H1172. http://dx.doi.org/10.1152/ajpheart.00464.2019.

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Insulin modulates vasomotor tone through vasodilator and vasoconstrictor signaling pathways. The purpose of the present work was to determine whether insulin-stimulated vasoconstriction is a pathophysiological phenomenon that can result from a combination of persistent insulin signaling, suppressed phosphatidylinositol-3 kinase (PI3K) activation, and an ensuing relative increase in MAPK/endothelin-1 (ET-1) activity. First, we examined previously published work from our group where we assessed changes in lower-limb blood flow in response to an oral glucose tolerance test (endogenous insulin sti

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4

Syuu, Yi, Hiromi Matsubara, Shingo Hosogi, and Hiroyuki Suga. "Pressor effect of electroacupuncture on hemorrhagic hypotension." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 285, no. 6 (2003): R1446—R1452. http://dx.doi.org/10.1152/ajpregu.00243.2003.

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Neiguan (PC-6) is a traditional acupoint in each forearm and overlies the trunk of the median nerve. Previous studies show that electroacupuncture (EA) at the Neiguan acupoint could improve not only myocardial ischemic dysfunction by inducing a depressor response but also recover hemorrhagic hypotension by inducing a pressor response. However, their physiological mechanisms are not yet elucidated. We investigated the pressor effect of Neiguan EA and its mechanism by focusing on left ventricular (LV) performance in a canine hemorrhagic hypotension model. We hemorrhaged 36 anesthetized and thora

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5

Cox, B. F., and V. S. Bishop. "Neural and humoral mechanisms of angiotensin-dependent hypertension." American Journal of Physiology-Heart and Circulatory Physiology 261, no. 4 (1991): H1284—H1291. http://dx.doi.org/10.1152/ajpheart.1991.261.4.h1284.

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We examined whether neural or humoral mechanisms mediate the acute versus chronic phases of angiotensin II (ANG II)-dependent hypertension in rabbits. ANG II was administered intravenously at 50 ng.kg-1.min-1 for 10 days. This dose of ANG II elevated mean arterial pressure (MAP) from 76 +/- 2 to 98 +/- 2 mmHg on day 1 and sustained the hypertension throughout the infusion period. Heart rate (226 +/- 7 beats/min) was not altered. The depressor response to ganglionic blockade (-38 +/- 2 mmHg) was significantly blunted on day 1 (-22 +/- 3 mmHg) and was significantly enhanced on days 5 (-52 +/- 4

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6

Guimond, J. G., M. R. Pinsky, and G. M. Matuschak. "Effect of synchronous increase in intrathoracic pressure on cardiac performance during acute endotoxemia." Journal of Applied Physiology 69, no. 4 (1990): 1502–8. http://dx.doi.org/10.1152/jappl.1990.69.4.1502.

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In the anesthetized closed-chest canine model of Gram-negative endotoxemia (n = 10), we tested the hypothesis that the effect of cardiac cycle-specific intrathoracic pressure pulses delivered by a heart rate-(HR) synchronized high-frequency jet ventilator (sync HFJV) on systolic ventricular performance is dependent on the level of preload. To control for HFJV frequency, hemodynamic responses were also measured at fixed frequency within 15% of HR (async HFJV). Biventricular stroke volumes (SV) were measured by electromagnetic flow probes. Measurements were made before (baseline) and 30 min afte

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7

Hicks, J. M., and A. P. Farrell. "The cardiovascular responses of the red-eared slider (Trachemys scripta) acclimated to either 22 or 5 degrees C. II. Effects of anoxia on adrenergic and cholinergic control." Journal of Experimental Biology 203, no. 24 (2000): 3775–84. http://dx.doi.org/10.1242/jeb.203.24.3775.

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Cardiovascular control in cold-acclimated freshwater turtles during chronic anoxic exposure is not well understood. We tested the hypothesis that the observed bradycardia in Trachemys scripta results from increased cholinergic inhibitory tone and reduced sympathetic activity. Cardiovascular status was measured in vivo in turtles acclimated to either 22 degrees C or 5 degrees C and either acutely exposed (6 h) to anoxia at 22 degrees C or chronically exposed (22 days) to anoxia at 5 degrees C. In 22 degrees C-acclimated turtles, injection of the cholinergic antagonist atropine induced a signifi

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8

Smith, Josh F., Hamish A. L. Lemmey, Lyudmyla Borysova, C. Robin Hiley, Kim A. Dora, and Christopher J. Garland. "Endothelial Nitric Oxide Suppresses Action-Potential-Like Transient Spikes and Vasospasm in Small Resistance Arteries." Hypertension 76, no. 3 (2020): 785–94. http://dx.doi.org/10.1161/hypertensionaha.120.15491.

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Endothelial dysfunction in small arteries is a ubiquitous, early feature of cardiovascular disease, including hypertension. Dysfunction reflects reduced bioavailability of endothelium-derived nitric oxide (NO) and depressed endothelium-dependent hyperpolarization that enhances vasoreactivity. We measured smooth muscle membrane potential and tension, smooth muscle calcium, and used real-time quantitative polymerase chain reaction in small arteries and isolated tubes of endothelium to investigate how dysfunction enhances vasoreactivity. Rat nonmyogenic mesenteric resistance arteries developed va

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9

Cox, B. F., and M. J. Brody. "Mechanisms of respiration-induced changes in vasomotor control exerted by rostral ventrolateral medulla." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 257, no. 3 (1989): R626—R634. http://dx.doi.org/10.1152/ajpregu.1989.257.3.r626.

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Efferent and afferent mechanisms involved in the differential depressor response to inactivating rostral ventrolateral medulla (RVLM) under conditions of normal (2.5 ml) and reduced (1.5 ml) tidal volume were examined in urethan-anesthetized rats. Under conditions of reduced tidal volume, bilateral microinjection of lidocaine (200 nl, 4%) into RVLM produced an attenuated fall in both mean arterial pressure (MAP) and renal sympathetic nerve activity (RSNA) despite the fact that base-line levels of both are unchanged. The specificity of the differential response was tested by examination of regi

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10

Tabrizchi, Reza, Kathryn A. King та Catherine C. Y. Pang. "Vascular role of vasopressin in the presence and absence of influence from angiotensin II or α-adrenergic system". Canadian Journal of Physiology and Pharmacology 64, № 8 (1986): 1143–48. http://dx.doi.org/10.1139/y86-194.

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The effects of a vasopressin (AVP) pressor antagonist, d(CH2)5Tyr(Me)AVP, on mean arterial pressure (MAP), total peripheral resistance (TPR), cardiac output (CO), and the distribution of CO were investigated by the microsphere technique in three groups of pentobarbital anesthetized rats: intact (I), saralasin pretreated (II), and phentolamine pretreated (III). Saralasin and phentolamine were infused intravenously to inactivate the renin–angiotensin and α-adrenergic systems, respectively. The AVP antagonist decreased MAP and TPR in all groups and it caused a greater depressor effect in groups I

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