Effects of Intravenous Clonidine on Ocular Blood Flow and Intraocular Pressure
Status:
Completed
Trial end date:
2005-01-01
Target enrollment:
Participant gender:
Summary
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.