Abstract

The effect of electrical stimulation of the facial nerve on ocular blood flow and intraocular pressure (IOP) was studied in monkeys, cats and rabbits. Ocular blood flow was determined with radioactive microspheres or by direct measurement of uveal blood flow from a cannulated vortex vein in rabbits. Frequency-response relationships were determined in monkeys (intraocular pressure) and rabbits (uveal blood flow). Stimulation of the facial nerve produced a marked increase (> 100%) in choroidal blood flow in all three species. The effect in the anterior uvea appeared the same, but less pronounced. Retinal blood flow was not affected by the stimulation in any of the species. In cats, local blood flow in the optic nerve was significantly increased by the stimulation. As there was no significant change in mean arterial blood pressure, the increase in blood flow must have been due to decreased vascular resistance. The uveal vasodilation was resistant to muscarinic blockade in all three species, excluding acetylcholine as the principal peripheral transmitter. Stimulation of the facial nerve also caused a moderate increase in IOP (range 1–11 cmH 2O), only investigated in monkeys. This increase in IOP seems to be secondary to the intraocular vasodilation. The maximal increase in intraocular pressure, in monkeys, and vasodilation, in rabbits, was obtained at 15–20 Hz. At these frequencies, the vasodilation was always abolished by ganglionic blockade. In rabbits, stimulation at high frequencies (> 40 Hz) sometimes produced uveal vasodilation even after ganglionic blockade. This vasodilation was always less pronounced than before the ganglionic blockade and could be abolished by muscarinic blockade. The increase in uveal blood flow, in rabbits, was not affected by administration of indomethacin, indicating that prostaglandins are not critically involved in the vasodilation produced by facial nerve stimulation. The vasodilatory nerve fibers in the facial nerve are likely to be involved in regulation of choroidal blood flow to control the environmental temperature for the retina. The present study establishes the existence of efferent vasodilatory nerve fibers of facial nerve origin to the uvea. The peripheral transmitter causing the vasodilation is suggested to be vasoactive intestinal polypeptide (VIP).

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