scholarly journals Changes in regional blood flow and cardiodynamics evoked by electrical stimulation of the fastigial nucleus in the cat and their similarity to orthostatic reflexes

1972 ◽  
Vol 227 (3) ◽  
pp. 729-747 ◽  
Author(s):  
Nobutaka Doba ◽  
Donald J. Reis
Keyword(s):  
Blood Flow ◽  
Electrical Stimulation ◽  
Regional Blood Flow ◽  
Fastigial Nucleus ◽  
Orthostatic Reflexes ◽  
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.

scholarly journals Electrical Stimulation of Cerebellar Fastigial Nucleus Reduces Ischemic Infarction Elicited by Middle Cerebral Artery Occlusion in Rat

1991 ◽  
Vol 11 (5) ◽  
pp. 810-818 ◽  
Author(s):  
Donald J. Reis ◽  
Scott B. Berger ◽  
Mark D. Underwood ◽  
Mazen Khayata
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Electrical Stimulation ◽  
Middle Cerebral Artery ◽  
Cerebral Artery ◽  
Fastigial Nucleus ◽  
Sprague Dawley ◽  
Cholinergic Mechanism ◽  
Ischemic Infarction ◽  
Stimulation Of

Electrical stimulation of the cerebellar fastigial nucleus (FN) globally and profoundly increases cerebral blood flow via a cholinergic mechanism. In cerebral cortex, the vasodilation is unassociated with alterations in cerebral glucose utilization, a condition favoring protection against cerebral ischemia. We sought to determine whether FN stimulation would modify the size of the focal ischemic infarction resulting from occlusion of the middle cerebral artery (MCA). The MCA was occluded in anesthetized rats of the spontaneously hypertensive (SHR) or Sprague-Dawley (SD) strains with or without 1 h of electrical stimulation of the FN. Twenty-four hours later, rats were killed and the volume of the infarction established in thionin-stained sections. In SHRs, FN stimulation reduced by 40% the well-established cortical and partially subcortical infarctions elicited by occlusion of the MCA (from 186 ± 35.2 to 113 ± 47.1 mm3, mean ± SD, n = 15; p < 0.001). The zone of retrieval was anatomically constant, consisting of a rim of cortex dorsal and ventral to the infarction and medially within the thalamus and striatum corresponding to the penumbral zone described by others. The effect was comparable in rats of the SD strain having smaller infarctions. The effect of FN stimulation appears to be selective for the FN system in that it is not evoked by stimulation of the dentate nucleus and is blocked by systemic administration of atropine (1.0 mg/kg). We conclude that excitation of an intrinsic system in brain represented in the rostral FN has the capacity to reduce substantially an ischemic infarction. Whether the result is a consequence of an action of the FN upon cerebral blood flow and/or results from protective actions of released transmitter is yet unknown.

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.

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.

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