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Effects of Latanoprost on Choroidal Blood Flow Regulation in Human Subjects
This study is currently recruiting participants.
Study NCT00712400   Information provided by Medical University of Vienna
First Received: July 8, 2008   No Changes Posted

July 8, 2008
July 8, 2008
June 2005
December 2008   (final data collection date for primary outcome measure)
Choroidal pressure-flow relationship [ Time Frame: in total 4 hours ] [ Designated as safety issue: No ]
Same as current
No Changes Posted
 
 
 
Effects of Latanoprost on Choroidal Blood Flow Regulation in Human Subjects
Effects of Latanoprost on Choroidal Blood Flow Regulation in Human Subjects

Latanoprost is a synthetic prodrug of 17-phenyl-substituted prostaglandin F2α analog. Used at a dose of one drop per day, it has been reported to produce a 30 to 35% reduction in intraocular pressure. Its mechanism of activation involves augmentation of the eye's natural uveoscleral outflow capacity .

There is evidence that ocular blood flow plays a role in the clinical course of glaucoma. Glaucoma medication that lowers IOP simultaneously increases ocular blood perfusion pressure, which in turn may increase ocular blood flow.

This could well contribute to the partially contradicting results concerning ocular hemodynamic effects of latanoprost. In vitro studies indicate that latanoprost has no effect on ocular vascular tone in therapeutical doses. By contrast, it has been reported in several studies that latanoprost 0.005% increases pulsatile ocular blood flow in patients with primary open angle glaucoma and normal tension glaucoma. This increase in pulsatile ocular blood flow mainly reflects an increase in the choroidal circulation.

Little is known about the potential effect of latanoprost on choroidal blood flow regulation in humans. The present study therefore tries to elucidate whether treatment with latanoprost may alter choroidal blood flow regulation during artificial changes in ocular perfusion pressure. In addition, the present study aims to clarify whether the change in choroidal blood flow after latanoprost administration are due to direct vasoactive effects or due to the increase in ocular perfusion pressure. The second alternative may have important implications on our understanding of glaucoma treatment, because reduction of IOP may then per se result in normalization of ocular blood flow regulation.

 
 
Interventional
Diagnostic, Randomized, Double Blind (Subject, Investigator), Parallel Assignment, Safety/Efficacy Study
  • Ocular Physiology
  • Intraocular Pressure
  • Regional Blood Flow
  • Drug: Latanoprost 0.005%, Xalatan®
  • Drug: Placebo
  • Active Comparator: Latanoprost 0.005%, Xalatan®
  • Placebo Comparator: Vehicle to latanoprost (eyedrops containing the same stabilizers as latanoprost, but no active drug)
 

*   Includes publications given by the data provider as well as publications identified by National Clinical Trials Identifier (NCT ID) in Medline.
 
Recruiting
32
February 2009
December 2008   (final data collection date for primary outcome measure)

Inclusion Criteria:

  • Men aged between 19 and 35 years, nonsmokers
  • Body mass index between 15th and 85th percentile (Must et al. 1991)
  • Normal findings in the medical history and physical examination unless the investigator considers an abnormality to be clinically irrelevant
  • Normal ophthalmic findings, ametropia < 3 dpt.

Exclusion Criteria:

  • Regular use of medication, abuse of alcoholic beverages, participation in a clinical trial in the 3 weeks preceding the study
  • Treatment in the previous 3 weeks with any drug
  • Symptoms of a clinically relevant illness in the 3 weeks before the first study day
  • History or presence of gastrointestinal, liver or kidney disease, or other conditions known to interfere with distribution, metabolism or excretion of study drugs
  • Blood donation during the previous 3 weeks
  • Ametropia >= 3 dpt
  • Iris bicolor
Male
19 Years to 35 Years
Yes
Contact: Gerhard Garhofer, MD 0043 1 40400 ext 2981 klin-pharmakologie@meduniwien.ac.at
Austria
 
NCT00712400
Gabriele Fuchsjäger-Mayrl; MD, Department of Clinical Pharmacology
OPHT-070703
Medical University of Vienna
 
 
Medical University of Vienna
July 2008

ICMJE     Data element required by the International Committee of Medical Journal Editors and the World Health Organization ICTRP