Abstract
ABSTRACT
Xylazine is an agent frequently used in combination with ketamine to anesthetize rabbits. Xylazine is also related pharmacologically to clonidine, a relatively selective α2-agonist. In the present studies, xylazine was examined for its effects on intraocular pressure (IOP) and pupil diameter (PD) in rabbits, cats and monkeys and on noradrenergic function in the cat nictitating membrane (CNM) preparation. Topical and unilateral administration of xylazine (1.0 mg) lowered IOP bilaterally in normal, unanesthetized rabbits, cats and monkeys and caused unilateral miosis in rabbits and cats. These ocular effects of xylazine were attenuated in superior cervical ganglionectomized (SX) cats and rabbits. In addition, intra-arterially administered xylazine (10, 33 and 100 μg) produced dose-related inhibition of contractions of the CNM elicited by electrically stimulating the pre- and postganglionic sympathetic trunks without altering the response to i.a. norepinephrine (10 μg). These data suggest that ocular effects of xylazine are mediated, in part, by alteration of sympathetic neuron function. Xylazine suppressed ocular hypertension induced by water loading and IOP recovery rate following hypertonic saline infusion in rabbits suggesting that aqueous flow was inhibited. Topical pretreatment with 0.05 mg of timolol caused potentiation of the ocular hypotensive response to 0.05 mg of xylazine in rabbits. These results indicate that xylazine lowers IOP, in part, by suppressing sympathetic neuronal function which causes a reduction in aqueous flow. The augmented response to timolol and xylazine, as compared with either agent alone, suggests a rational basis for combining a prejunctionally active agent with a postjunctionally active one.
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