Abstract
In rabbits intracranial stimulation of the oculomotor nerve causes vasoconstriction in the anterior uvea and vasodilation in the choroid and an attempt has been made to analyze the mechanism involved in the vasoconstrictive response to stimulation. The oculomotor nerve was stimulated unilaterally, and regional blood flow was determined in both eyes using radioactively labelled microspheres. Hexamethonium bromide, in a dose of 40–80 mg/kg body weight, completely abolished the vasoconstrictive response in the iris and the ciliary processes. The blood flow in all parts of the uvea tended to be higher on the stimulated side than on the control side. The parasympatholytic agent biperiden lactate, in a dose of 2·5–5 mg/kg body weight, reduced the response in the iris, but no significant change was observed in the ciliary processes. The alpha-adrenergic blocking agent phentolamine chloride, in a dose of 10–15 mg/kg body weight had no significant effect on the response in the iris but reversed the effect in the ciliary processes. A combination of biperiden and phentolamine totally abolished the vasoconstrictive response in the iris, and there was increased blood flow in the ciliary processes on the stimulated side. The results indicate that intracranial stimulation of the oculomotor nerve and possibly of adjacent structures caused a release of vasodilating and vasoconstricting agents in the uvea. The vasoconstrictive effect was partly muscarinic, possibly due to miosis, and partly due to stimulation of receptors sensitive to phentolamine. A ganglion or ganglion-like receptors, somewhere between the site of stimulation and the effector cells, seem to be involved in the transmission of the vasoconstrictive impulses.
Published Version
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