Effects of antiglaucoma drugs on ocular hemodynamics in healthy volunteers.
OBJECTIVE
There is evidence that ocular blood flow plays a critical role in the clinical course of glaucoma. Hence a reduction in ocular blood flow due to topical antiglaucoma treatment should be avoided. The purpose of this study was to characterize the effect of antiglaucoma drugs on ocular hemodynamics.


METHODS
In a double-blind, placebo-controlled, randomized crossover study, we investigated the effects of single topical doses of five beta-blocking agents (befunolol, betaxolol, levobunolol, metipranolol, and timolol), two adrenergic agents (clonidine and dipivefrin [INN, dipivefrine]), and a parasympathomimetic agent (pilocarpine) on ocular and systemic hemodynamics in healthy subjects (n = 10). Fundus pulsation amplitudes in the macula and the optic disc were measured to characterize pulsatile choroidal and optic disc blood flow, respectively. Moreover, central retinal and ophthalmic artery blood flow velocities were measured by Doppler ultrasound.


RESULTS
Befunolol, metipranolol, timolol, clonidine, and dipivefrin reduced fundus pulsations in the macula and the optic disc (-9% to -14% versus baseline). In contrast, betaxolol, levobunolol, and pilocarpine had no effect on fundus pulsations. Antiglaucoma drugs had no effect on either blood flow velocities in the central retinal or the ophthalmic artery or systemic hemodynamics.


CONCLUSIONS
Our results indicate that befunolol, metipranolol, timolol, clonidine, and dipivefrin reduce choroidal and optic disc blood flow. This could be caused by drug diffusion to the choroid, which may cause vasoconstriction. Ocular blood flow reduction was not observed with betaxolol, levobunolol, or pilocarpine. The lack of effect of all drugs under study on central retinal blood flow velocity might partially be the result of autoregulative mechanisms. Because optic nerve head blood flow likely plays a critical role in the clinical course of glaucoma, the use of antiglaucoma drugs, which reduce blood flow, should be reconsidered.
Schmetterer
L
L
Department of Clinical Pharmacology, Vienna University School of Medicine, Austria.
Strenn
K
K
Findl
O
O
Breiteneder
H
H
Graselli
U
U
Agneter
E
E
Eichler
H G
HG
Wolzt
M
M
D018663:Adrenergic Agents / Q000008:administration & dosage / Q000494:pharmacology* / Q000627:therapeutic use; D000319:Adrenergic beta-Antagonists / Q000008:administration & dosage / Q000494:pharmacology* / Q000627:therapeutic use; D000328:Adult; D000704:Analysis of Variance; D001783:Blood Flow Velocity / Q000187:drug effects; D002829:Choroid / Q000098:blood supply; D018592:Cross-Over Studies; D004311:Double-Blind Method; D005123:Eye / Q000098:blood supply*; D005654:Fundus Oculi; D005901:Glaucoma / Q000097:blood / Q000188:drug therapy; D006439:Hemodynamics / Q000187:drug effects*; D006801:Humans; D008297:Male; D009880:Ophthalmic Artery / Q000187:drug effects / Q000502:physiology; D009898:Optic Disk / Q000098:blood supply; D010277:Parasympathomimetics / Q000008:administration & dosage / Q000494:pharmacology* / Q000627:therapeutic use; D010862:Pilocarpine / Q000008:administration & dosage / Q000494:pharmacology* / Q000627:therapeutic use; D011673:Pulsatile Flow / Q000187:drug effects; D012039:Regional Blood Flow / Q000187:drug effects; D012171:Retinal Vessels / Q000187:drug effects / Q000502:physiology; D018608:Ultrasonography, Doppler
D018663:Adrenergic Agents; D000319:Adrenergic beta-Antagonists; D010277:Parasympathomimetics; D010862:Pilocarpine