Search

The effects of bimatoprost on aqueous humor dynamics were quantified in monkey eyes. Uveoscleral outflow was measured by the anterior chamber perfusion method, using FITC-dextran. Total outflow facility was determined by the two-level constant pressure method. Aqueous flow was measured with a scanning ocular fluorophotometer. Uveoscleral outflow was 0.96 +/- 0.19 muL min(-1) in vehicle-treated eyes and 1.37 +/- 0.27 muL min(-1) (n = 6; P < .05) in eyes that received bimatoprost 0.01% b.i.d. x 5 days. Bimatoprost had no effect on total outflow facility, which was 0.42 +/- 0.05 muL min(-1) at baseline and 0.42 +/- 0.04 muL min(-1) after bimatoprost treatment. Bimatoprost had no significant effect on aqueous humor flow. This study demonstrates that bimatoprost increases uveoscleral outflow but not total outflow facility or aqueous humor flow, indicating that it lowers intraocular pressure in ocular normotensive monkeys by a mechanism that exclusively involves uveoscleral outflow.

The effects of bimatoprost on aqueous humor dynamics were quantified in monkey eyes. Uveoscleral outflow was measured by the anterior chamber perfusion method, using FITC-dextran. Total outflow facility was determined by the two-level constant pressure method. Aqueous flow was measured with a scanning ocular fluorophotometer. Uveoscleral outflow was 0.96 +/- 0.19 muL min(-1) in vehicle-treated eyes and 1.37 +/- 0.27 muL min(-1) (n = 6; P < .05) in eyes that received bimatoprost 0.01% b.i.d. x 5 days. Bimatoprost had no effect on total outflow facility, which was 0.42 +/- 0.05 muL min(-1) at baseline and 0.42 +/- 0.04 muL min(-1) after bimatoprost treatment. Bimatoprost had no significant effect on aqueous humor flow. This study demonstrates that bimatoprost increases uveoscleral outflow but not total outflow facility or aqueous humor flow, indicating that it lowers intraocular pressure in ocular normotensive monkeys by a mechanism that exclusively involves uveoscleral outflow.

The effects of bimatoprost on aqueous humor dynamics were quantified in monkey eyes. Uveoscleral outflow was measured by the anterior chamber perfusion method, using FITC-dextran. Total outflow facility was determined by the two-level constant pressure method. Aqueous flow was measured with a scanning ocular fluorophotometer. Uveoscleral outflow was 0.96 +/- 0.19 muL min(-1) in vehicle-treated eyes and 1.37 +/- 0.27 muL min(-1) (n = 6; P < .05) in eyes that received bimatoprost 0.01% b.i.d. x 5 days. Bimatoprost had no effect on total outflow facility, which was 0.42 +/- 0.05 muL min(-1) at baseline and 0.42 +/- 0.04 muL min(-1) after bimatoprost treatment. Bimatoprost had no significant effect on aqueous humor flow. This study demonstrates that bimatoprost increases uveoscleral outflow but not total outflow facility or aqueous humor flow, indicating that it lowers intraocular pressure in ocular normotensive monkeys by a mechanism that exclusively involves uveoscleral outflow.

The effects of bimatoprost on aqueous humor dynamics were quantified in monkey eyes. Uveoscleral outflow was measured by the anterior chamber perfusion method, using FITC-dextran. Total outflow facility was determined by the two-level constant pressure method. Aqueous flow was measured with a scanning ocular fluorophotometer. Uveoscleral outflow was 0.96 +/- 0.19 muL min(-1) in vehicle-treated eyes and 1.37 +/- 0.27 muL min(-1) (n = 6; P < .05) in eyes that received bimatoprost 0.01% b.i.d. x 5 days. Bimatoprost had no effect on total outflow facility, which was 0.42 +/- 0.05 muL min(-1) at baseline and 0.42 +/- 0.04 muL min(-1) after bimatoprost treatment. Bimatoprost had no significant effect on aqueous humor flow. This study demonstrates that bimatoprost increases uveoscleral outflow but not total outflow facility or aqueous humor flow, indicating that it lowers intraocular pressure in ocular normotensive monkeys by a mechanism that exclusively involves uveoscleral outflow.

The effects of bimatoprost on aqueous humor dynamics were quantified in monkey eyes. Uveoscleral outflow was measured by the anterior chamber perfusion method, using FITC-dextran. Total outflow facility was determined by the two-level constant pressure method. Aqueous flow was measured with a scanning ocular fluorophotometer. Uveoscleral outflow was 0.96 +/- 0.19 muL min(-1) in vehicle-treated eyes and 1.37 +/- 0.27 muL min(-1) (n = 6; P < .05) in eyes that received bimatoprost 0.01% b.i.d. x 5 days. Bimatoprost had no effect on total outflow facility, which was 0.42 +/- 0.05 muL min(-1) at baseline and 0.42 +/- 0.04 muL min(-1) after bimatoprost treatment. Bimatoprost had no significant effect on aqueous humor flow. This study demonstrates that bimatoprost increases uveoscleral outflow but not total outflow facility or aqueous humor flow, indicating that it lowers intraocular pressure in ocular normotensive monkeys by a mechanism that exclusively involves uveoscleral outflow.