Role of Adenosine in the Control of Choroidal Blood Flow During Changes in Ocular Perfusion Pressure.
Autoregulation is the ability of a vascular bed to maintain blood flow despite changes in perfusion pressure. For a long time it had been assumed that the choroid is a strictly passive vascular bed, which shows no autoregulation. However, recently several groups have identified some autoregulatory capacity of the human choroid. In the brain and the retina the mechanism behind autoregulation is most likely linked to changes in transmural pressure. In this model arterioles change their vascular tone depending on the pressure inside the vessel and outside the vessel. In the choroid, several observations argue against a direct involvement of arterioles. However, the mechanism behind choroidal autoregulation remains unclear. Adenosine, an endogenous purine metabolic end product with a potent vasodilatory effect on multiple vascular beds, leads to an increase in retinal and choroidal vessel diameter. The present study aims to investigate whether adenosine plays a role in choroidal autoregulation during a decrease in ocular perfusion pressure, which will be achieved by an increase in intraocular pressure.
Pressure/flow relationships will be investigated in the absence and presence of adenosine.
|Study Design:||Allocation: Randomized
Intervention Model: Crossover Assignment
Masking: Double (Participant, Investigator)
Primary Purpose: Treatment
|Official Title:||Role of Adenosine in the Control of Choroidal Blood Flow During Changes in Ocular Perfusion Pressure.|
- choroidal pressure-flow relationship [ Time Frame: 2 hours at 2 study days ]
|Study Start Date:||January 2005|
|Study Completion Date:||April 2005|
|Primary Completion Date:||April 2005 (Final data collection date for primary outcome measure)|
|Active Comparator: 1||Drug: Adenosine|
|Placebo Comparator: 2||Drug: Placebo|
Please refer to this study by its ClinicalTrials.gov identifier: NCT00712764
|Department of Clinical Pharmacology, Medical University of Vienna|
|Vienna, Austria, 1090|
|Principal Investigator:||Michael Wolzt, MD||Department of Clinical Pharmacology, Medical University of Vienna|