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The effect of stimulating the greater superficial petrosal nerve (g.s.p.n.) upon retroglenoid venous blood flow has been tested in anaesthetized, paralysed and artificially ventilated rats. In 11 out of 15 tests, blood flow increased by an average of 25% with a time to peak response of 28 s. This response was abolished with the injection of atropine 0.1 mg kg-1 injected intra-arterially. With both petrosal nerves intact, the administration of 6-7% CO2 in air or 15% O2 in N2 caused average increases in blood flow of 105% and 45% respectively. These responses were not affected by bilateral section of the g.s.p.n. Similar experiments were carried out in 5 anaesthetized, spontaneously breathing rabbits in which, in addition to PaCO2 and PaO2, PO2, PCO2 and blood flow in the caudate nucleus were measured continuously using chronically implanted mass spectrometer catheters and heated thermistors. Caudate nucleus blood flow increased in response to hypoxia and hypercapnia and this response was not significantly affected by section of one or both g.s.p.n., sinus or vagus nerves. With section of sinus and vagus nerves, blood flow changed passively with arterial pressure.

The application of cobalt chloride to the peripheral cut end of the greater superficial petrosal nerve (g.s.p.n.) in rats revealed that only a few fibers in the plexus of nerves on the adventitial surface of the internal carotid artery were in axonal continuity with the g.s.p.n. A similarly small contribution of cholinergic fibers to cerebral blood vessels from this nerve was suggested by the observation that section of the g.s.p.n. resulted in an insignificant reduction in the density of the AChE-staining plexus in the internal carotid and cerebral arteries and in the incidence of at most 2% degenerate terminals of those observed on the middle cerebral artery. Alternative explanations of the results are discussed: that the AChE-staining fibers are postganglionic, that the time course for degeneration is unusually slow and that non-cholinergic fibers stain non-specifically for AChE. It is concluded that a cholinergic dilator pathway is most probably carried by the g.s.p.n. but that it is not unique.