Abstract
Abstract: :
Purpose: To test the hypothesis that topical brimonidine is a vasoconstrictor which contributes to its ocular hypotensive effect. Methods: The study used pentobarbital anesthetized rabbits in which mean arterial pressure (MAP), intraocular pressure (IOP) and orbital venous pressure (OVP) were measured by direct cannulation. In Group 1 (n=11), aqueous flow was measured by fluorophotometry. In Group 2 (n=11), ciliary blood flow, carotid blood flow and heart rate were measured by laser Doppler flowmetry, transit-time flowmetry and a cardiotachometer, respectively. Measurements in both groups were made for 60 – 90 min before and after topical brimonidine (60 µg). Group 2 underwent mechanical MAP manipulations to quantify effects on the ciliary pressure-flow relation. In Group 3 (n=6), episcleral venous pressure (EVP) was measured by direct cannualtion with a micropipette-based servo-null system during the initial brimonidine response. Results: Brimonidine had minor effects on MAP (-4%, p<0.5), carotid blood flow (-14%, p>0.05) and heart rate (-7%, p<0.01), and large effects on IOP (-32%, p<0.01), aqueous flow (-47%, p<0.01) ciliary blood flow (-37%, p<0.01) and EVP (-42%, p<0.05). Brimonidine also shifted the ciliary pressure-flow relation and the heart rate baroreflex function curve downward. Conclusions: In anesthetized rabbits, topical brimonidine is a vasoconstrictor that decreases ciliary blood flow and EVP as well as aqueous production. The decrease in aqueous flow and EVP contribute to brimonidine's ocular hypotensive effect. Ciliary underperfusion may cause the decreased aqueous production. Topical brimonidine inhibits baroreflex control of heart rate indicating systemic absorption.
Keywords: inflow/ciliary body • outflow: trabecular meshwork • blood supply