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

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.

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Hemodynamic effects of electrical stimulation of forebrain angiotensin and osmosensitive sites

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.1978.235.4.h445 ◽

1978 ◽

Vol 235 (4) ◽

pp. H445-H451 ◽

Cited By ~ 5

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.

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

Neurophysiology ◽

10.1007/bf01093387 ◽

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

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Chronotropic, inotropic, and coronary artery blood flow responses to stimulation of specific canine sympathetic nerves and ganglia

Canadian Journal of Physiology and Pharmacology ◽

10.1139/y84-229 ◽

1984 ◽

Vol 62 (11) ◽

pp. 1374-1381 ◽

Cited By ~ 8

Author(s):

R. D. Janes ◽

D. E. Johnstone ◽

J. A. Armour

Keyword(s):

Blood Flow ◽

Electrical Stimulation ◽

Coronary Blood Flow ◽

Stellate Ganglion ◽

Sympathetic Nerves ◽

Neural Stimulation ◽

Intramyocardial Pressure ◽

Intact Heart ◽

Cardiac Nerves ◽

Stimulation Of

Electrical stimulation of the major sympathetic cardiac nerves and ganglia in chloralose-anesthetized, open-chest dogs elicited specific changes in heart rate, coronary blood flow, regional intramyocardial pressure, or intraventricular pressure. The effects produced by stimulation of a cardiac nerve were similar to, but never greater than those produced by stimulation of the ipsilateral stellate ganglion. Coronary blood flow was increased when neural stimulation increased intramyocardial pressure. In contrast, coronary blood flow was not altered significantly when neural stimulation induced tachycardia without increasing intramyocardial pressure. It is concluded that in the intact heart, electrical stimulation of the sympathetic cardiac nerves or ganglia increases coronary blood flow by augmenting intramyocardial pressure, not chronotropism.

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Cerebral blood flow during fastigial pressor response in cats

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.1990.258.3.h729 ◽

1990 ◽

Vol 258 (3) ◽

pp. H729-H733

Author(s):

J. L. Williams ◽

M. A. Murray ◽

K. A. Schalk ◽

D. D. Heistad

Keyword(s):

Blood Flow ◽

Cerebral Blood Flow ◽

Arterial Pressure ◽

Severe Hypertension ◽

Pressor Response ◽

Sympathetic Nerves ◽

Fastigial Nucleus ◽

Acute Hypertension ◽

Cervical Sympathetic ◽

Stimulation Of

We tested the hypotheses that electrical stimulation of the fastigial nucleus increases cerebral blood flow by a dilator mechanism, impairs autoregulation during increases in arterial pressure, and attenuates increases in cerebral blood flow during acute hypertension by activation of sympathetic nerves. Cerebral blood flow was measured with microspheres in anesthetized cats during control and moderate or severe hypertension produced by stimulation of the rostral fastigial nucleus. Cervical sympathetic nerves to one cerebral hemisphere were cut to compare responses in the innervated and denervated hemispheres. Fastigial stimulation at a level that raised arterial pressure from 94 +/- 10 (mean +/- SE) to 133 +/- 6 mmHg had no significant effect on cerebral blood flow. Autoregulation was preserved because cerebral vascular resistance increased approximately 40% during the fastigial pressure response. When mean arterial pressure was raised to 189 +/- 9 mmHg by stimulation of the fastigial nucleus, cerebral blood flow increased similarly in the denervated hemisphere and the hemisphere with intact sympathetic nerves. We conclude that stimulation of the fastigial nucleus in cats does not have a direct dilator effect on cerebral vessels, does not impair autoregulation during moderate hypertension, and does not attenuate increases in cerebral blood flow during severe hypertension by activation of sympathetic pathways.

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

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.1989.257.1.h297 ◽

1989 ◽

Vol 257 (1) ◽

pp. H297-H304 ◽

Cited By ~ 1

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.

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Cerebrovascular effects produced by electrical stimulation of fastigial nucleus

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.1991.261.3.h707 ◽

1991 ◽

Vol 261 (3) ◽

pp. H707-H713 ◽

Cited By ~ 1

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.

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