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December 1994

Phalloidin Inhibits Epinephrine's and Cytochalasin B's Facilitation of Aqueous Outflow

Author Affiliations

From the Department of Ophthalmology and Visual Sciences, University of Wisconsin, Madison. The authors have no proprietary or commercial interest related to the subject matter in the manuscript.

Arch Ophthalmol. 1994;112(12):1610-1613. doi:10.1001/archopht.1994.01090240116035

Objective:  To determine whether phalloidin, a fungal peptide that inhibits actin filament depolymerization, could inhibit the ability of cytochalasin B and epinephrine to increase the facility of aqueous outflow in the eyes of living cynomolgus monkeys.

Methods:  Outflow facility was determined by two-level constant-pressure perfusion of the anterior chamber. After measurement of baseline facility in both eyes, one eye of each animal received intracameral phalloidin (1.3, 13, or 130 μmol/L); the opposite eye received vehicle. Both eyes then received either epinephrine (0.3 mmol/L) or cytochalasin B (0.2 mmol/L), and facility was again measured.

Results:  Cytochalasin B and epinephrine increased facility by 120% to 190% and 100% to 180%, respectively (uncorrected for 15% resistance washout caused by perfusion itself). Phalloidin itself (13 or 130 μmol/L) did not affect facility, but it inhibited up to 50% of the facility-increasing effect of cytochalasin B and epinephrine.

Conclusions:  We conclude that (1) the aqueous humor outflow facilitating effects of cytochalasin B or epinephrine depend in some manner on depolymerization of actin filaments within trabecular meshwork cells, and (2) actin filaments may help regulate aqueous outflow.

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