| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
|
|
|
|||||||
|
|||||||||
From the Department of Ophthalmology, Herlev Hospital, University of Copenhagen, Denmark.
PURPOSE. To investigate the effect of the carbonic anhydrase inhibitor acetazolamide (AZM) on passive permeability and active transport of fluorescein across the blood-retina barrier in healthy subjects. The study may have implications for the understanding of the edema-reducing effect of AZM.
METHODS. The effect of AZM on the blood-retina barrier function was assessed by differential vitreous spectrofluorometry using fluorescein as a tracer. The study included fourteen healthy subjects in a randomized double-masked crossover trial with 3 days’ treatment with AZM (500 mg/d) and placebo, respectively. The two examinations were separated by at least 1 week. Fluorescein concentration was determined separately from its metabolite fluorescein glucuronide. The passive permeability of fluorescein was determined by computerized modeling and curve-fitting to the preretinal curve and the plasma concentration curve obtained at 30 to 60 minutes after the injection of fluorescein. The unidirectional permeability due to outward active transport from vitreous to blood was estimated from the preretinal gradient and the plasma concentration at 7 to 10 hours after injection.
RESULTS. Treatment with AZM was associated with significant increases in passive permeability and unidirectional permeability of fluorescein. For the passive permeability the increase was on average 0.3 ± 0.4 nm/s (mean ± SD; range, -0.8–1.0 nm/s), and for the unidirectional permeability the increase was on average 7.4 nm/s ± 7.0 (mean ± SD; range, -3.3–19.0 nm/s).
CONCLUSIONS. Acetazolamide caused an increase in passive permeability. Unidirectional permeability was increased by AZM, indicating a stimulation of the outward active transport of fluorescein. It has been proposed that the edema-reducing effect of AZM is due to stimulated ion and fluid removal from the retina to the choroid. The results of this study are consistent with AZM affecting the blood-retina barrier with stimulation of at least one ion transport mechanism.
This article has been cited by other articles:
|
|
 |
|
  B. Sander, D. N. Thornit, L. Colmorn, C. Strom, A. Girach, L. D. Hubbard, H. Lund-Andersen, and M. Larsen Progression of Diabetic Macular Edema: Correlation with Blood Retinal Barrier Permeability, Retinal Thickness, and Retinal Vessel Diameter Invest. Ophthalmol. Vis. Sci., September 1, 2007; 48(9): 3983 - 3987. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
C. Strom, B. Sander, K. Klemp, L. P. Aiello, H. Lund-Andersen, and M. Larsen Effect of Ruboxistaurin on Blood-Retinal Barrier Permeability in Relation to Severity of Leakage in Diabetic Macular Edema Invest. Ophthalmol. Vis. Sci., October 1, 2005; 46(10): 3855 - 3858. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 B. Moldow, M. Larsen, B. Sander, and H. Lund-Andersen Passive permeability and outward active transport of fluorescein across the blood-retinal barrier in early ARM Br. J. Ophthalmol., May 1, 2001; 85(5): 592 - 597. [Abstract] [Full Text]
|
|
|
|
|
|
B. Sander, M. Larsen, B. Moldow, and H. Lund-Andersen Diabetic Macular Edema: Passive and Active Transport of Fluorescein through the Blood-Retina Barrier Invest. Ophthalmol. Vis. Sci., February 1, 2001; 42(2): 433 - 438. [Abstract] [Full Text]
|
|
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
