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Activation of a cranial vasodilator pathway during seizures in rats
Journal article   Peer reviewed

Activation of a cranial vasodilator pathway during seizures in rats

Frank M Faraci, Michael G Motley and Donald D Heistad
The American journal of physiology, Vol.251(5 Pt 2), pp.H969-H975
11/1986
DOI: 10.1152/ajpheart.1986.251.5.H969
PMID: 2877585

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Abstract

The purpose of this study was to determine whether seizures, which activate sympathetic nerves, also activate a vasodilator pathway to extracranial tissues of the head. Blood flow was measured with microspheres during control conditions and seizures in anesthetized, paralyzed rats. Seizures were produced by bicuculline or pentylenetetrazole. During seizures in rats with intact sympathetic nerves, blood flow to masseter muscle decreased and blood flow to tongue did not change. Following bilateral cervical sympathetic denervation or high spinal cord section, seizure produced marked increases in blood flow to masseter and tongue. These vasodilator responses, which were confined to the cephalic circulation (and were not observed in biceps femoris) were blocked by hexamethonium. The vasodilator response to seizures in masseter and tongue was not significantly attenuated after atropine. Thus seizures activate a dilator pathway to extracranial tissue of the head, sympathetic nerves limit the increase in blood flow produced by activation of the cranial dilator pathway during seizures, and vasodilatation in masseter and tongue during seizures is mediated primarily by a noncholinergic mechanism.
 Cerebrovascular Circulation - drug effects Rats Atropine - pharmacology Male Sympathetic Nervous System - physiopathology Rats, Inbred Strains Seizures - chemically induced Hexamethonium Compounds - pharmacology Microspheres Seizures - physiopathology Animals Pentylenetetrazole Spinal Cord - physiopathology Vasodilation - drug effects Hexamethonium Bicuculline

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