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Vol. 280, Issue 1, 454-459, 1997
Department of Pharmacology and Therapeutics (J.P.D.L.C.,
F.S.d.l.C.) and
Department of Ophthalmology (A.M., M.M., J.M.G.C.),
School of Medicine, University of Málaga, Málaga, Spain
Platelet hyperactivity has been one of the mechanisms implicated in the
pathogenesis of diabetic retinopathy. Antiplatelet agents have been
shown, in experimental models, to prevent the development of retinal
vascular abnormalities when given from the first day after the onset of
diabetes. We assessed the effect of aspirin plus dipyridamole (6 + 12 mg/kg daily) on the retinal vascular pattern in experimental
streptozotocin-induced diabetes in rats, when the treatment was given
at different intervals after the induction of diabetes, over a 3-month
study period. Saline-pretreated diabetic rats showed a time-dependent
increase in the platelet production of thromboxane B2
(r = 0.981, P < .0001) and a decrease in the
aortic production of 6-keto-PGF1
. The percentage of retinal area occupied by horseradish peroxidase-labeled vessels decreased progressively in relation to the length of time of the evolution of diabetes (r = 0.983, P < .00001) and
the thromboxane/prostacyclin ratio. Treatment with aspirin plus
dipyridamole caused an inhibition of the platelet production of
thromboxane B2 and a decrease in the vascular synthesis of
prostacyclin. Treatment with antiplatelet agents slowed down the
decrease in the percentage of retinal area occupied by horseradish
peroxidase-labeled vessels. These data provide further evidence to
support the results of previous clinical trials in which antiplatelet
agents had a beneficial effect on the evolution of retinal lesions in
early diabetic retinopathy.
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K. Yamashiro, A. Tsujikawa, S. Ishida, T. Usui, Y. Kaji, Y. Honda, Y. Ogura, and A. P. Adamis Platelets Accumulate in the Diabetic Retinal Vasculature Following Endothelial Death and Suppress Blood-Retinal Barrier Breakdown Am. J. Pathol., July 1, 2003; 163(1): 253 - 259. [Abstract] [Full Text] [PDF] |
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