Abstract:
To assess the effects of systemic, non–selective alpha adrenergic blockade with phentolamine on ocular hydrodynamics. This study used pentobarbital anesthetized rabbits in which mean arterial pressure (MAP) and intraocular pressure (IOP) were measured by direct cannulation. In Group 1 (n=7), aqueous flow was measured by fluorophotometry. In Group 2 (n=11), ciliary blood flow was measured by laser Doppler flowmetry (LDF). In some animals (n=7), the facial vein was cannulated to measure cranial venous pressure (Pv); in others, choroidal blood flow was measured by LDF (n=3). Measurements were made before and after administration of phentolamine (0.1 mg/kg, iv).
The decrease in IOP was always preceded slightly by a decrease in venous pressure. The decrease in IOP was also associated with transient increases in ciliary and choroidal blood flow. A dose of phentolamine with a modest (albeit significant) effect on blood pressure has unexpectedly complex effects on ocular hydrodynamics. The initial IOP decrease is too fast to be explained by aqueous dynamics or ocular rigidity, and so is most likely due to disgorgement of blood volume such as occurs with choroidal vasoconstrictors like L–NAME. However, during the initial IOP drop, ciliary and choroidal blood flow both increase, consistent with blocked alpha constrictor tone. What then explains the rapid IOP drop? The intriguing piece of evidence is the decrease in venous pressure, consistent with the venous vasodilation and increased compliance downstream from the eye that could occur with alpha blockade. Thus, a tentative hypothesis for the initial IOP drop is the drop in venous pressure outside the eye permitting easier egress of blood from the choroidal veins. The sustained ocular hypotensive effect is explained by the decrease in aqueous production, and perhaps a decrease in episcleral venous pressure.
Keywords: aqueous • ciliary body • blood supply