The enucleated arterially perfused cat eye. I. Effects on protein permeability.

Protein permeability of the ciliary epithelium of enucleated arterially perfused cat eyes was studied. Tracer concentrations of 125I-albumin, in an arterial perfusate solution consisting of a balanced salt solution (BSS) without added colloid, was found in the anterior chamber fluid (AH) in a percentage similar to the AH/plasma ratio found for protein in the living cat eye. Stimulation of AH formation by acetylcholine plus eserine increased protein permeability markedly and by a similar amount in eyes perfused either with BSS or with 100% serum. These data indicate that arterial perfusion of the enucleated eye with BSS alone induces no gross abnormality of the blood-aqueous barrier.

Clonidine.

Clonidine hydrochloride has been demonstrated to produce vasoconstriction in the anterior segment of the cat eye. The mode of this action has been found to be due to direct stimulation of alpha-adrenergic receptors. In the intact, enucleated, arterially perfused eye, clonidine was found to decrease the rate of aqueous humor production. We suggest that clonidine, like hydroxyamphetamine hydrobromide, phenylephrine hydrochloride, and dopamine hydrochloride, decreases aqueous humor formation by constriction of afferent ciliary process blood vessels.

The pressure dependency of aqueous humor formation in the anesthetized cat.

In cats anesthetized with pentobarbital Na, a highly significant correlation was found between the rate of aqueous humor production and eye arterial perfusion pressure (blood pressure minus intraocular pressure). The filtration coefficient for water was 0.312 microliter min-1 mm Hg-1. This value is not significantly different from those reported earlier for enucleated, arterially perfused eyes of the same species.

Ciliary ganglion stimulation. II. Neurogenic, intraocular pathway for excitatory effects on aqueous humor production and outflow.

Data obtained suggest that preganglionic stimulation of the ciliary ganglion produces an increase of aqueous humor formation and of facility of outflow "C" through the following neurogenic pathway: (1) the preganglionic fibers synapse in the ciliary ganglion as evidenced by depression of the response with nicotine applied topically to the ganglion. (2) The impulse proceeds to the equivalent of an intraocular interneuron which can be blocked by low concentrations of atropine and has been previously identified as being an E-2 receptor site. (3) From the interneuron, activity is ultimately exerted without further synapse on alpha-adrenergic receptors through the release of norepinephrine from the neuronal terminals. The adrenergic mechanism of action is supported by the inhibition of the responses by phenoxybenzamine, bretylium, and guanethidine. Constriction of efferent ciliary process blood vessels by neuron-released norepinephrine seems to be the end effect responsible for the increased production of aqueous humor. The site of the end response to increase "C" is unclear.

Ciliary ganglion stimulation. I. Effects on aqueous humor inflow and outflow.

Stimulation of the ciliary ganglion in an enucleated, arterially perfused cat eye preparation produced a sustained increase in aqueous humor formation and an increase in the rate of aqueous humor outflow. The increased aqueous humor formation induced by ciliary ganglion stimulation has been found to be pressure-dependent and therefore suggests that ultrafiltration may be the underlying mechanism of action. No change in capillary permeability of the ciliary body could be demonstrated.