Effects of Intravenous Clonidine on Ocular Blood Flow and Intraocular Pressure
Background Clonidine, a derivate of Imidazol, is an antihypertensive drug. It acts by stimulating adrenergic receptors on nerves in the brain and Imidazol-receptors. As a result, clonidine slows the heart rate and reduces blood pressure. Clonidine was approved by the FDA in 1974 and is registered in Austria with the brand name “Catapresan”.
Alpha2 adrenergic agonists are nowadays used topically as eye drops in glaucoma treatment. In addition to their known effect of lowering intraocular pressure, alpha2 adrenoceptor agonists are neuroprotective. Brimonidine, which is the most commonly used topical alpha-2 agonist, is currently on the market for treatment of glaucoma and is effective in reducing intraocular pressure. It has, however, been shown that brimonidine is a very potent vasoconstrictor in the ciliary body thus reducing aqueous humor production. Little is, however, known about potential vasoconstrictor effects of brimonidine in the posterior pole of the eye. This is of clinical importance, because optic nerve head ischemia appears to contribute to glaucoma pathophysiology. Direct investigation of the ocular hemodynamic effects of brimonidine is, however, difficult, because lowering intraocular pressure with brimonidine may confound the results due to the concomitant change in ocular perfusion pressure.
The aim of the present study is to assess the effect of intravenous clonidine as model drug of alpha agonists on ocular blood flow and IOP in healthy humans.
To investigate effects of clonidine on ocular blood flow and intraocular pressure.
|Study Design:||Allocation: Randomized
Endpoint Classification: Efficacy Study
Intervention Model: Crossover Assignment
Primary Purpose: Treatment