Characteristics of facial nerve-elicited cerebral vasodilatation determined using laser Doppler flowmetry.

Cerebral cortical perfusion was monitored continuously with laser Doppler flowmetry and quantitative measurements of cerebral blood flow performed with the freely diffusible tracer 4-iodo[N-methyl-14C]antipyrine in the alpha-chloralose-anesthetized cat. The facial nerve was isolated from the brain stem via a posterior fossa craniotomy and electrically stimulated at frequencies of 1, 2, 5, 10, and 20 s-1. A stimulus-locked frequency-dependent increase in cerebral perfusion was seen in the parietal cortex; the mean maximum increase was 91 +/- 22% at 20 s-1. This compared with an absolute flow of 116 +/- 3 ml.100 g-1.min-1 at the same site. In addition, the response was associated with a marked increase in cerebral venous O2 content indicating that it is a primary neurogenic dilator response. This response could be blocked by hexamethonium but not by atropine and was thus mediated by an autonomic ganglion but not by the classical muscarinic postsynaptic receptor. Sectioning of the facial nerve did not alter cerebrovascular reactivity to hypercapnia. These data confirm the vasodilator effect of activation of the facial nerve and document its mediation through an intermediate parasympathetic ganglion. Consistent with previous data, the facial nerve does not appear to play a role in hypercapnic cerebral vasodilatation. Furthermore, this study highlights the usefulness of laser Doppler flowmetry in the cerebral circulation and in particular in the setting where repeated measures are required, such as in pharmacological studies.