Cholinergic vasoconstrictor effects in the rabbit eye: vasomotor effects of pentobarbital anesthesia

Oculomotor nerve stimulation causes vasoconstriction in the anterior uvea, which is due partly to a muscarinic mechanism and partly to a non-sympathetic aminergic mechanism. The labelled microsphere method was used to analyze the effect of pentobarbital anesthesia on the resting cholinergic vasomotor tone in the anterior uvea and to determine the relationship between stimulation frequency and vasomotor response. An attempt was made also to ascertain whether the aminergic part of the vasoconstriction is caused by release of 5-hydroxytryptamine or norepinephrine. Induction of pentobarbital anesthesia caused a marked vasodilation in the iris and the ciliary processes and a subsequent muscarinic blockade had no effect on the blood flow. A similar result was obtained in the optic nerve. In the choroid plexus, heart muscle, pineal body and coecum, pentobarbital anesthesia caused vasodilation and a subsequent muscarinic blockade caused vasoconstriction. In the brain pentobarbital anesthesia caused a marked reduction in the blood flow of the grey matter and a moderate reduction in the white matter. After a muscarinic blockade there was some increase in the blood flow of the grey matter. Stimulation of the oculomotor nerve caused near maximum vasomotor responses at 10-20 Hz; maximum effect on the pupil size was obtained at 40-50 Hz. Depletion of 5-hydroxytryptamine with fenfluramine did not prevent the aminergic part of the vasoconstriction and a marked vasoconstriction was also observed after pretreatment with reserpine. The results indicate the pentobarbital anesthesia abolishes most of the spontaneous cholinergic vasoconstrictor tone of the anterior uvea and that the aminergic part of the oculomotor nerve induced vasoconstriction is caused by the stimulation of phentolamine-sensitive receptors by a mechanism probably not involving release of norepinephrine or 5-hydroxytryptamine.