1 Endothelins (ETs) might play a pathophysiological role in a variety of vascular diseases. The aim of the present study was to characterize the eects of BQ-123, a speci®c ET A receptor antagonist on systemic and renal haemodynamics in healthy subjects. This was done at baseline and during infusion of exogenous ET-1. 2 The study was performed in a balanced, randomized, placebo-controlled, double blind 4 way crossover design in 10 healthy male subjects. Subjects received co-infusions of ET-1 (2.5 ng kg 71 min 71 for 120 min) or placebo and BQ-123 (15 mg min 71 for 60 min and subsequently 60 mg min 71 for 60 min) or placebo. Renal plasma¯ow (RPF) and glomerular ®ltration rate (GFR) were assessed by the paraaminohippurate (PAH) and the inulin plasma clearance method, respectively. 3 BQ-123 alone had no renal or systemic haemodynamic eect. ET-1 signi®cantly reduced RPF (724%, P50.001) and GFR (712%, P=0.034). These eects were abolished by co-infusion of either dose of BQ-123 (RPF: P=0.0012; GFR: P=0.020). 4 BQ-123 reversed the renal haemodynamic eects induced by exogenous ET-1 in vivo. This indicates that vasoconstriction in the kidney provoked by ET-1 is predominantly mediated by the ET A receptor subtype.

The amount of LCD detected by PCI was approximately the same with all IOL types (approximately 20%) except the PhacoFlex SI30 with a capsular tension ring (10%).

Background and Purpose-The acetazolamide provocation test is commonly used to study cerebrovascular vasomotor reactivity. On the basis of the effect of a carbonic anhydrase inhibitor in the central nervous system, we hypothesized that acetazolamide may also increase blood flow in the human choroid. Methods-In a placebo-controlled, randomized, double-blind, three-way crossover design, acetazolamide (500 mg or 1000 mg IV) or placebo was administered to nine healthy subjects. The effect of acetazolamide was studied at 15-minute intervals for 90 minutes. Pulsatile choroidal blood flow was assessed with laser interferometric measurement of fundus pulsation. In addition, mean blood flow velocity and resistive index in the ophthalmic artery were measured with Doppler sonography. In a second study in six healthy subjects, we assessed the effect of acetazolamide (1000 mg IV) on intraocular pressure. Results-Acetazolamide increased fundus pulsation amplitude in a dose-dependent manner (1000 mg: ϩ33%; 500 mg: ϩ20%; PϽ0.001, ANOVA). The effect of acetazolamide on MFV (1000 mg: ϩ18%; 500 mg: ϩ8%; Pϭ0.003, ANOVA) and RI (1000 mg: Ϫ4%; 500 mg: Ϫ2%; Pϭ0.006, ANOVA) was less pronounced but also significant. Acetazolamide did not induce any changes in systemic hemodynamic parameters but significantly decreased intraocular pressure (1000 mg: Ϫ37%; PϽ0.0001). Conclusions-The present data show for the first time that intravenously administered acetazolamide increases choroidal blood flow in humans. This phenomenon therefore indicates that the acetazolamide provocation test may qualify as a tool to investigate ocular vasomotor reactivity in a variety of ocular diseases. Moreover, the increase in choroidal blood flow after carbonic anhydrase inhibition can be expected to contribute to the therapeutic efficacy of carbonic anhydrase inhibitors in glaucoma. (Stroke. 1998;29:997-1001.)