PURPOSE:Topically-applied dopamine antagonists reduce intraocular pressure (IOP) and inrease retinal blood flow in animal models. We examined the acute effects of intravenous infusion of a dopamine blocker (droperidol) on these parameters in healthy humans. METHODS:Sixteen subjects free from ocular or systemic disease (mean age 33 +/- 10 yrs) received either 5 mg i.v. droperidol over 5 minutes, or i.v. saline placebo in double-masked fashion. IOP was determined 30 and 60 minutes later, while color Doppler imaging was used to determine flow velocities in the ophthalmic, central retinal, and nasal and temporal posterior ciliary arteries 60 minutes after drug infusion. RESULTS: 30 minutes after drug infusion, IOP was reduced 6.0 mmHg as compared with baseline (p<0.001); after 60 minutes, IOP remained reduced by 3.7 mmHg (p<0.001). Placebo had no effect on IOP. While droperidol slightly elevated blood pressure and increased the calculated ocular perfusion pressure, the drug reduced visual acuity and contrast sensitivity (p<0.05). Droperidol elevated peak systolic velocity in the central retinal and nasal posterior ciliary arteries, without changing end-diastolic velocity or the resistance index in either of these vessels. Droperidol had no effect on flow velocities in the ophthalmic artery or the temporal posterior ciliary artery. CONCLUSIONS: The rapid and marked ocular hypotension resulting from intravenous droperidol suggests that this agent may prove useful in the management of acute ocular hypertension. The retrobulbar changes consequent to the ocular tension reduction likely represent autoregulatory responses to altered ocular perfusion pressure.
RCT Entities:
PURPOSE: Topically-applied dopamine antagonists reduce intraocular pressure (IOP) and inrease retinal blood flow in animal models. We examined the acute effects of intravenous infusion of a dopamine blocker (droperidol) on these parameters in healthy humans. METHODS: Sixteen subjects free from ocular or systemic disease (mean age 33 +/- 10 yrs) received either 5 mg i.v. droperidol over 5 minutes, or i.v. saline placebo in double-masked fashion. IOP was determined 30 and 60 minutes later, while color Doppler imaging was used to determine flow velocities in the ophthalmic, central retinal, and nasal and temporal posterior ciliary arteries 60 minutes after drug infusion. RESULTS: 30 minutes after drug infusion, IOP was reduced 6.0 mmHg as compared with baseline (p<0.001); after 60 minutes, IOP remained reduced by 3.7 mmHg (p<0.001). Placebo had no effect on IOP. While droperidol slightly elevated blood pressure and increased the calculated ocular perfusion pressure, the drug reduced visual acuity and contrast sensitivity (p<0.05). Droperidol elevated peak systolic velocity in the central retinal and nasal posterior ciliary arteries, without changing end-diastolic velocity or the resistance index in either of these vessels. Droperidol had no effect on flow velocities in the ophthalmic artery or the temporal posterior ciliary artery. CONCLUSIONS: The rapid and marked ocular hypotension resulting from intravenous droperidol suggests that this agent may prove useful in the management of acute ocular hypertension. The retrobulbar changes consequent to the ocular tension reduction likely represent autoregulatory responses to altered ocular perfusion pressure.