Control of Ocular Blood Flow

The eye has a dual vascular supply. The uveal vessels are distributed within the choroid, the ciliary body, and the iris; and the retinal vessels within the inner parts of the retina. The vascularization of the uvea is very rich and the blood flow is high, which stabilizes the temperature of the eye. The vascularization of the retina is relatively sparse, which is an obvious advantage for the optics. The perfusion pressure in the eye can be defined as the local arterial blood pressure minus the intraocular pressure. Reductions in perfusion pressure, caused by increments in intraocular pressure, or reductions in mean arterial pressure reduce the blood flow in the choroid. In the retina, there are efficient autoregulatory mechanisms that prevent changes in flow within a wide range of perfusion pressures. Stimulation of the cervical sympathetic chain causes vasoconstriction in the uvea, with near-maximal effects as 10 Hz. The sympathetic nerves are not activated during moderate hemorrhage. They apparently prevent overperfusion and breakdown of intraocular barriers under conditions of acute elevation of the arterial blood pressure. Electrical stimulation of the oculomotor nerve causes cholinergic vasoconstriction in the anterior uvea. Near-maximal vasoconstriction is obtained between 10 and 20 Hz. In conscious animals, muscarinic blockade causes vasodilatation in the iris, indicating that there is a basal traffic in the vasomotor fibers of the oculomotor nerve. Electrical stimulation of the facial nerve causes vasodilatation in the uvea that cannot be prevented by muscarinic blockade: near-maximal vasodilatation is obtained between 10 and 20 Hz. Vasoactive intestinal polypeptide is probably the transmitter that mediates the response to stimulation of the facial nerves.