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Effects of nimodipine on cerebral vasoconstrictor responses

Effects of nimodipine on cerebral vasoconstrictor responses (4). Studies in vitro have demonstrated that nimodipine inhibits calcium influx into cerebral vascular muscle prevents contraction induced by several agents including serotonin, norepinerine, histamine, potassium (6, 23-25). Thus it seemed probable that constriction of cerebral vessels in vivo would be inhibited by nimodipine. In this study we examined effects of nimodipine on cerebral in vivo. Two approaches were used. In one series of experiments, pial artery diameter was measured during several stimuli. We examined to sympathetic nerve stimulation, acute hypertension, hypocapnia. Our hypothesis was that, if extracellular calcium is the primary source of calcium during of cerebral arteries, nimodipine might inhibit to several types of stimuli. In a second series of studies, we measured cerebral blood flow with microseres to determine whether nimodipine impairs autoregulation of cerebral flow. The goal of these studies was to determine whether inhibition by nimodipine of pial artery vasoconstriction during increases in arterial pressure is accompanied by corresponding impairment of autoregulation of blood flow. METHODS sympathetic stimulation; autoregulation; hypocapnia; cats; cynomolgusmonkeys Measurement of Pial Artery Diameter nimodipine has been shown to have direct effects on cerebral vessels. Nimodipine produces dilatation of pial arteries in cats in vivo (2, 14, 22) modest increases http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png AJP - Heart and Circulatory Physiology The American Physiological Society

Effects of nimodipine on cerebral vasoconstrictor responses

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Publisher
The American Physiological Society
Copyright
Copyright © 1984 the American Physiological Society
ISSN
0363-6135
eISSN
1522-1539
Publisher site
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Abstract

(4). Studies in vitro have demonstrated that nimodipine inhibits calcium influx into cerebral vascular muscle prevents contraction induced by several agents including serotonin, norepinerine, histamine, potassium (6, 23-25). Thus it seemed probable that constriction of cerebral vessels in vivo would be inhibited by nimodipine. In this study we examined effects of nimodipine on cerebral in vivo. Two approaches were used. In one series of experiments, pial artery diameter was measured during several stimuli. We examined to sympathetic nerve stimulation, acute hypertension, hypocapnia. Our hypothesis was that, if extracellular calcium is the primary source of calcium during of cerebral arteries, nimodipine might inhibit to several types of stimuli. In a second series of studies, we measured cerebral blood flow with microseres to determine whether nimodipine impairs autoregulation of cerebral flow. The goal of these studies was to determine whether inhibition by nimodipine of pial artery vasoconstriction during increases in arterial pressure is accompanied by corresponding impairment of autoregulation of blood flow. METHODS sympathetic stimulation; autoregulation; hypocapnia; cats; cynomolgusmonkeys Measurement of Pial Artery Diameter nimodipine has been shown to have direct effects on cerebral vessels. Nimodipine produces dilatation of pial arteries in cats in vivo (2, 14, 22) modest increases

Journal

AJP - Heart and Circulatory Physiology – The American Physiological Society

Published: Aug 1, 1984

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