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      Effect of Trimetazidine on Retinal Ischemia/Reperfusion Injury in Rats


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          Purpose: To investigate the effect of trimetazidine (TMZ), an antioxidant agent, on the ischemia/reperfusion (I/R) injury in rat retina histopathologically. Methods: The retinal I/R model was carried out by the 4-vessel occlusion method on Wistar albino rats. Twenty-one rats were divided into 7 groups, each comprising 3 rats. The animals in groups 1, 2 and 3 underwent 30 min of ischemia + 4 h of reperfusion and were treated by the administration of saline, TMZ before reperfusion and TMZ before ischemia, respectively. The animals in groups 4, 5 and 6 underwent 90 min of ischemia + 4 h of reperfusion and were treated in the same way as those in groups 1, 2 and 3, respectively. The 7th group was sham operated. Results: Thirty and 90 min of ischemia followed by 4 h of reperfusion induced retinal injury in the rat retina. Histopathologically, the inner plexiform and inner nuclear layers were the most affected parts. TMZ was able to reduce almost all retinal I/R damage when administered before ischemia. A cytoprotective effect of TMZ was partly observed in those animals which were treated before reperfusion. Conclusion: TMZ seemed to have a protective effect against retinal I/R injury in rats.

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          Most cited references6

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          Retinal ischemia induced by occlusion of both common carotid arteries in rats as demonstrated by electroretinography.

          In 2 models of reduced cerebral blood flow-permanent occlusion of the vertebral arteries plus transient occlusion of the common carotid arteries (4VO) and transient clamping of the common carotid arteries (BCCA)-the acute effects on the electrical function of the retina were monitored by recording the photopic electroretinogram. During both 4VO and BCCA the amplitude of the b-wave was reduced. Within 30 min of reperfusion after 4VO and after BCCA the b-wave had fully recovered. In contrast, the a-wave was not affected by either treatment. The data suggest that occlusion of common carotid arteries leads to retinal ischemia and might represent a useful model of amaurosis fugax.
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            Oxygen free radicals adversely affect the regulation of vascular tone by nitric oxide in the rabbit retina under high intraocular pressure.

            Flash electroretinograms (ERG) were recorded in the rabbit eye submitted to high intraocular pressure (HIOP) induced by the suction-cup method. When intraocular pressure rose to 100 mmHg, ERG was suppressed but rapidly recovered even under HIOP when animals were pre-treated either intravitreously with a nitric oxide donor, sodium nitroprusside, or intravenously with free radical scavengers, superoxide dismutase (SOD)+catalase. In contrast, injection of a nitric oxide synthesis inhibitor, nitro-L-arginine, into the vitreous cavity inhibited the protective effect of SOD+catalase during HIOP-induced ERG extinction. These results suggest that nitric oxide could play a role in the regulation of ocular vessel tone and that severe ischemia can impede this effect through oxygen-derived free radical generation.
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              Hydroxyl radical generation in the cat retina during reperfusion following ischemia.

              There is increasing evidence that oxygen-derived free radicals are generated during the early phase of reperfusion, and account for part of the damage caused by transient ischemia in various tissues. To study this in the retina, cats were injected intravenously with sodium salicylate (100 mg kg-1), which reacts as a hydroxyl radical trap to form 2,3- and 2,5-dihydroxybenzoic acids (DHBA). Thirty minutes following injection, the retina of one eye of each animal was subjected to ischemia by intraocular pressure elevation via cannulation of the anterior chamber, while the fellow eye served as a sham-operated control. Ischemia was induced for 60 min (six eyes) and 90 min (eight eyes) followed by 5 min of reperfusion. In six other eyes, ischemia was induced for 90 min without reperfusion. After enucleation, the retinas were immediately removed, placed in ice-cold buffer and the retinal levels of 2,3- and 2,5-DHBA were quantitated by high pressure liquid chromatography, coupled with electrochemical detection. Results were normalized and expressed as ng DHBA microgram-1 salicylate mg-1 retinal protein. After 60 min of ischemia followed by reperfusion the normalized levels of 2,3- and 2-5-DHBA were no different in the experimental and control retinas. However, the levels of both 2,3- and 2,5-DHBA were significantly higher in the retinas subjected to 90 min ischemia followed by reperfusion than in the control tissues (P = 0.012 and P = 0.036, n = 8 respectively). Following 90 min ischemia without reperfusion, the normalized dihydroxybenzoate levels in the retinas were no higher than in their controls.(ABSTRACT TRUNCATED AT 250 WORDS)

                Author and article information

                S. Karger AG
                August 2001
                31 May 2001
                : 215
                : 4
                : 309-317
                aDepartment of Ophthalmology, Pamukkale University Medical School, Denizli, and bDepartment of Histology, Hacettepe University Medical School, Ankara, Turkey
                50880 Ophthalmologica 2001;215:309–317
                © 2001 S. Karger AG, Basel

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                Page count
                Figures: 12, References: 30, Pages: 9
                Original Paper · Travail original · Originalarbeit

                Vision sciences,Ophthalmology & Optometry,Pathology
                Retinal ischemia/reperfusion,Trimetazidine,Rat retina


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