Physiology Clinical Trial
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.
Study objectives:
To investigate effects of clonidine on ocular blood flow and intraocular pressure.
n/a
Allocation: Randomized, Endpoint Classification: Efficacy Study, Intervention Model: Crossover Assignment, Masking: Double-Blind, Primary Purpose: Treatment
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