Sympathetic Denervation Effects on Avian Eye Development and Aqueous Fluid Dynamics 1

Abstract

Sympathetic denervation of the eye in experimental mammals, either by surgical means (1, 2) , or pharmacologically (3), has been reported to cause a decrease in intraocular pressure (IOP), an increase in outflow facility (C) (1, 2), no change (4) or a decrease (5) in aqueous secretion, no change in episckral venoaq pressure (4, mydriasis (6) or miosis (7) , suparsensitivity to alphaadrenergic drugs (7), decreased vascular tone and increased blood flow to the anterior segment of the eye (4, 8). Many of these effects are transient, the peak response occurring about 1 day after anterior cervical ganglionectomy. This “24-hr ganglionectomy effect” has been attributed to the release of stored catecholamines, primarily norepinephrine, from degenerating postganglionic nerve terminals (1, 9). This hypothesis was strengthened by Eakins and Eakins (10), and by Sears et al. (11), who showed that catecholamine stores in the weal tissues were depleted over a time period which coincided with postganglionectomy changes in IOP and C.

There are conflicting reports regarding the long-term effects of ganglionectomy on the eye: a recturn to normal may occur within 3 days (2), especially after unilateral rather than bilateral ganglionectomy. However, Sears et al. (11) reported that, following a transient rise, outflow facility was greatly reduced for almost 4 weeks after unilateral ganglionectomy, and C did not return to normal until 12 weeks after bilateral sympathetic dmervation. Langham (7) found that supersensitivity to norepinephrine was still evident 8 days after unilateral ganglionectomy, and in the experiments of Holland and Mimhls (3), miosis during the first 48 hr was followed by mydriasis lasting as long as 5 weeks in chemically sympathectomized monkeys. From the reduced IOP and increased C, these authors postulated that postganglionectomy effects were accoqpanied by reduced intraocular pressure and miosis (3).