The effect of electrical stimulation of vestibular-complex formations on systemic arterial pressure and regional blood flow

1971 ◽  
Vol 2 (1) ◽  
pp. 26-32
Author(s):  
A. I. Vyshatina
Keyword(s):  
Blood Flow ◽  
Electrical Stimulation ◽  
Arterial Pressure ◽  
Regional Blood Flow ◽  
Systemic Arterial Pressure ◽  
Vestibular Complex ◽  
Complex Formations ◽  
Stimulation Of

Hemodynamic effects of electrical stimulation of forebrain angiotensin and osmosensitive sites

1978 ◽  
Vol 235 (4) ◽  
pp. H445-H451 ◽  
Keyword(s):  
Blood Flow ◽  
Electrical Stimulation ◽  
Arterial Pressure ◽  
Median Eminence ◽  
Regional Blood Flow ◽  
Renal Hypertension ◽  
Brain Structures ◽  
Ventromedial Hypothalamus ◽  
Pressure Changes ◽  
Stimulation Of

Previous studies from this laboratory have indicated an important role for angiotensin-sensitive anteroventral third ventricular (AV3V) brain structures in normal regulation of arterial pressure and development of renal hypertension. The present experiments examined the effects of electrical stimulation of these periventricular areas on arterial pressure and regional blood flow in the anesthetized rat. Electrodes were placed in the AV3V region 3–10 days prior to acute studies. Blood flow was measured in extracorporeal blood flow circuits. Electrical stimulation produced only small changes in arterial pressure. Despite the small pressure changes, stimulation caused marked frequency-dependent alterations in regional blood flow. Renal and splanchnic flows were reduced while hindlimb flow was increased. Resistance changes were abolished by surgical denervation or ganglionic blockade but were unaffected by adrenalectomy. Hemodynamic responses to AV3V stimulation were abolished by a lesion in the area of the median eminence. It may be concluded that AV3V stimulation, through activation of pathways descending through the ventromedial hypothalamus-median eminence region, produces profound regional blood flow shifts without greatly altering arterial pressure.

Rebound cardiovascular responses following stimulation of canine vagosympathetic complexes or cardiopulmonary nerves

1985 ◽  
Vol 63 (9) ◽  
pp. 1122-1132 ◽  
Author(s):  
J. A. Armour ◽  
W. C. Randall
Keyword(s):  
Electrical Stimulation ◽  
Arterial Pressure ◽  
Cardiovascular System ◽  
Cardiovascular Responses ◽  
Systemic Arterial Pressure ◽  
Cardiac Responses ◽  
Stimulation Of

Electrical stimulation of a canine vagosympathetic complex or a cardiopulmonary nerve can elicit a variety of negative chronotropic and inotropic cardiac responses, with or without alterations in systemic arterial pressure. In the period immediately following cessation of such a stimulation "rebound" tachycardia, increased inotropism above control values in one or more regions of the heart, and (or) elevation in systemic arterial pressure can occur. These "rebound" phenomena are abolished by propranolol or ipsilateral chronic sympathectomy. It is proposed that "vagal" poststimulation "rebound" of the canine cardiovascular system is primarily the result of activation of sympathetic neural elements present in the vagosympathetic complexes or cardiopulmonary nerves.

Hemodynamic basis of oscillations in systemic arterial pressure in conscious rats

1995 ◽  
Vol 269 (1) ◽  
pp. H62-H71 ◽  
Author(s):  
B. J. Janssen ◽  
J. Oosting ◽  
D. W. Slaaf ◽  
P. B. Persson ◽  
H. A. Struijker-Boudier
Keyword(s):  
Blood Flow ◽  
Cardiac Output ◽  
Arterial Pressure ◽  
Renal Blood Flow ◽  
Regional Blood Flow ◽  
Systemic Arterial Pressure ◽  
Hemodynamic Pattern ◽  
Cross Correlation Analysis ◽  
Vascular Beds ◽  
Phase Angles

In conscious resting rats, beat-to-beat fluctuations in systemic mean arterial pressure (MAP) were compared with those in cardiac output and those in blood flow in the renal, mesenteric, and hindquarter vascular beds. Spontaneous oscillations (lability) in MAP were observed in frequency bands centered about 1.6 Hz (high: HF), 0.4 Hz (mid: MF), and 0.13 Hz (low: LF). Lability of MAP was confined within the LF (approximately 8 s) band. Lability of cardiac output, on the other hand, showed primary HF oscillations. LF oscillations in regional blood flow were most prominent in the mesenteric and renal vascular beds. In these beds, LF oscillations in blood flow showed negative phase angles with MAP, whereas those between MAP and hindquarter blood flow were positive. Cross correlation analysis indicated that approximately 2 s following a LF change in MAP, LF changes in mesenteric and renal blood flow occurred opposite to those of MAP. Changes in hindquarter flow were negatively correlated with those in MAP about zero time delay. Admittance gains were > or = 1 across all frequencies for all vascular beds, indicating the absence of autoregulation. This hemodynamic pattern suggests that myogenic mechanisms predominantly control mesenteric and renal blood flow in a nonautoregulatory but rather superregulatory manner, while autonomic mechanisms regulate hindquarter blood flow. Thus, in conscious resting rats, spontaneous fluctuations in systemic arterial pressure predominantly exhibit slow (approximately 8 s) oscillations, which do not arise from fluctuations in cardiac output, but originate from regionally specific myogenic oscillatory mechanisms contributing to resistance to flow.

Effects of stimulation of fastigial nucleus on cerebral blood flow in cats

1989 ◽  
Vol 257 (1) ◽  
pp. H297-H304 ◽  
Author(s):  
J. L. Williams ◽  
D. D. Heistad ◽  
J. L. Siems ◽  
W. T. Talman
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Electrical Stimulation ◽  
Arterial Pressure ◽  
Blood Gases ◽  
Vessel Diameter ◽  
Fastigial Nucleus ◽  
Cross Sectional ◽  
Doppler Probe ◽  
Stimulation Of

The goal of this study was to examine effects of electrical stimulation of the rostral fastigial nucleus on cerebral blood flow. Anesthetized cats were studied, and arterial pressure and blood gases were maintained at control levels during fastigial stimulation. In one group, we measured vessel diameter and velocity of blood flow through a pial artery with a Doppler probe and calculated blood flow as the product of cross-sectional area and velocity. Electrical stimulation of the fastigial nucleus produced a small increase in pial arterial flow of 16 +/- 6% (means +/- SE, P less than 0.05). Pial vascular resistance increased during moderate hypertension and decreased during decreases in arterial pressure, which indicates that cerebral vascular responses were not impaired. In a second group, cerebral blood flow was measured with microspheres. Blood flow to the pons and medulla increased 25 +/- 11 and 21 +/- 11%, respectively, during stimulation of the fastigial nucleus, but blood flow to the cerebral cortex did not increase significantly. Stimulation produced decreases in flow to the renal cortex and duodenum of 39 +/- 10 and 39 +/- 15%, respectively, and flow to the heart increased 48 +/- 22%, which indicates that the stimulus was efficacious. Thus electrical stimulation of the rostral fastigial nucleus in cats elicits only a small increase in cerebral blood flow.

Uterine arterial vasoconstrictions mediated by ovarian nerves in virgin and postpartum rats

1997 ◽  
Vol 272 (1) ◽  
pp. R318-R325 ◽  
Author(s):  
S. M. Hutchison ◽  
A. E. Tietz ◽  
K. A. Trostel ◽  
L. P. Schramm
Keyword(s):  
Blood Flow ◽  
Electrical Stimulation ◽  
Arterial Pressure ◽  
Uterine Artery ◽  
Sympathetic Nerves ◽  
Adrenergic Blockade ◽  
Sympathetic Vasoconstriction ◽  
Femoral Vessels ◽  
Ovarian Nerves ◽  
Stimulation Of

In most mammals, including humans, pregnancy results in the loss of most uterine vasomotor fibers. These experiments determined whether, despite this denervation, sympathetic nerves mediated uterine vasoconstrictions in the rat 24 h after delivery. Both virgin and uniparous postpartum rats were anesthetized with urethan. Femoral vessels were cannulated for measurement of arterial pressure and intravenous administration of fluids and drugs. Blood flow was measured in a uterine artery after ligation of all anastomotic ovarian vessels. Electrical stimulation of ovarian nerve efferents elicited frequency-dependent uterine vasoconstrictions in both virgin and postpartum rats. Vasoconstrictions in postpartum rats were not significantly different from those observed in virgins. In both virgin and postpartum rats, neurogenic vasoconstrictions were reduced by combined alpha 1- and alpha 2-adrenergic blockade. We conclude that the uterine branches of the ovarian nerve mediate adrenergic uterine vasoconstrictions. In the largely denervated uterus of the postpartum rat, these vasoconstrictions may be mediated by surviving innervation of the uterine artery and its major branches. Sympathetic vasoconstriction acting at these sites would constitute an effective defense against postpartum hemorrhage.

Cerebrovascular effects produced by electrical stimulation of fastigial nucleus

1991 ◽  
Vol 261 (3) ◽  
pp. H707-H713 ◽  
Author(s):  
W. T. Talman ◽  
D. M. Dragon ◽  
D. D. Heistad ◽  
H. Ohta
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Electrical Stimulation ◽  
Arterial Pressure ◽  
Vascular Resistance ◽  
Fastigial Nucleus ◽  
Vascular Effect ◽  
Metabolic Mechanism ◽  
Alpha Chloralose ◽  
Stimulation Of

We used the microsphere technique and laser flowmetry to assess cerebral blood flow in 43 anesthetized rats. Cerebral blood flow did not increase significantly when the fastigial nucleus was stimulated 15 min after administration of alpha-chloralose. In animals that received maintenance doses of alpha-chloralose, the modest (50%) increase in cerebral blood flow that did occur returned toward control during stimulation despite a continued stable elevation of arterial pressure. Stimulation of fastigial nucleus 2 h after alpha-chloralose elicited a 20 +/- 3 mmHg increase in arterial pressure; cerebral blood flow increased gradually for 30-60 s after the rise in arterial pressure and reached a peak that was approximately 90% (P less than 0.05) above baseline. The stimuli did not significantly reduce vascular resistance or impair autoregulation. We did not stimulate the fastigial nucleus for more than 2 h after administration of alpha-chloralose because anesthesia was effective for only 2 h. This study demonstrates that stimulation of the fastigial nucleus in rat produces a delayed increase in cerebral blood flow that is blocked by alpha-chloralose anesthesia. The delay in increases of cerebral blood flow suggests that a metabolic mechanism, not a direct neurogenic vascular effect, may account for increases in flow with fastigial stimulation.

Electrical stimulation of the carotid sinus lowers arterial pressure and improves heart rate variability in l-NAME hypertensive conscious rats

2020 ◽  
Vol 43 (10) ◽  
pp. 1057-1067 ◽  
Author(s):  
Gean Domingos-Souza ◽  
Fernanda Machado Santos-Almeida ◽  
César Arruda Meschiari ◽  
Nathanne S. Ferreira ◽  
Camila A. Pereira ◽  
...  
Keyword(s):  
Heart Rate ◽  
Heart Rate Variability ◽  
Electrical Stimulation ◽  
Arterial Pressure ◽  
Carotid Sinus ◽  
Conscious Rats ◽  
Stimulation Of
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