Circulation Research, Vol 72, 470-475, Copyright © 1993 by American Heart Association
ARTICLES |
M Nakai, K Tamaki, J Ogata, Y Matsui and M Maeda
National Cardiovascular Center Research Institute, Osaka, Japan.
Functional studies have yet to be undertaken to establish which brain region subserves the parasympathetic regulation of the cerebral circulation. Using 31 anesthetized rats with precluded cervical sympathetic trunks, we therefore attempted to perform chemical stimulation of the greater petrosal nerve (GPN) cell group, which is a subgroup of the superior salivatory nucleus and sends off axons largely to the parasympathetic pterygopalatine ganglion via the GPN component of the facial nerve. The cerebrocortical blood flow was monitored with a laser-Doppler flowmeter. Unilateral stimulation of the GPN cell group by microinjection of L-glutamate reduced the ipsilateral cerebrocortical vascular resistance, maximally by 16.4 +/- 4.1% (mean +/- SD, n = 61). The response was not mediated by the classic muscarinic receptors of the cerebral vessel wall. However, pharmacological blockade of the peripheral parasympathetic ganglia and acute and chronic bilateral removal of the parasympathetic postganglionic fibers originating in the pterygopalatine ganglion abolished the response. The present data thus provide functional evidence that the GPN cell group may constitute a parasympathetic cerebrovasodilator center.
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