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Biomedical subjects

F J Macri

Publications and source records attributed to F J Macri.

11 recordsLinked to original sources
PubMed1978

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.

Animals↗
PubMed1975

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.

Acetylcholine↗
PubMed1975

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.

Acetylcholine↗