P 351 Monosialoganglioside GM1 reduces ischemia-reperfusion induced injury in the rat retina

Weber, Michel; Mohand‐Saïd, Saddek; Lignereux, F.; Péchereau, A.; Sahel, J; Dreyfus, H.

doi:10.1016/0042-6989(95)90611-8

Cited by 15 publications

(24 citation statements)

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“…On the one hand, as in earlier studies [9][10][11], we observed that pressure-induced retinal ischemia in the rat eye causes a decrease in thickness and loss of cells of the inner retina. The IPL thickness was the most reduced (70%) and provided a sensitive indication of neuronal damage in the adjacent nucleated layers.…”

Section: Discussionsupporting

confidence: 69%

Protective Effect of Trimetazidine in a Model of Ischemia-Reperfusion in the Rat Retina

Mohand‐Saïd¹,

Jacquet²,

Lucien³

et al. 2002

Ophthalmic Res

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Trimetazidine is an anti-ischemic agent which is frequently prescribed as a prophylactic treatment of episodes of angina pectoris and as a symptomatic treatment of vertigo and tinnitus. It has also shown beneficial effects in models of visual dysfunction, but the mechanism(s) by which this occurs is as yet undefined. The present study was intended to evaluate the influence of trimetazidine on retinal damage induced by ischemia-reperfusion in a rat model. Retinal ischemia was induced by increasing intraocular pressure to 160 mm Hg for 60 min. Trimetazidine or buffer controls were administered 3 days before the ischemia or in the postischemic period. The degree of retinal damage was assessed after 15 and 30 days of reperfusion after the ischemic insult by histopathologic study according to Hughes’ quantification of ischemic damage. Retinal ischemia led to significant reductions in thickness and cell number, mainly in the inner retinal layers. The results from the study demonstrate that treatment with intraperitoneally injected trimetazidine conferred significant protection against retinal ischemic damage. Better results were obtained in the pretreatment group after 15 days of reperfusion. Trimetazidine protects the rat retina from pressure-induced ischemic injury and might be considered a potential therapeutic modality for combating retinal ischemia.

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Section: Discussionsupporting

confidence: 69%

Protective Effect of Trimetazidine in a Model of Ischemia-Reperfusion in the Rat Retina

Mohand‐Saïd¹,

Jacquet²,

Lucien³

et al. 2002

Ophthalmic Res

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“…26,27 The thickness of the IPL, INL, ONL, and the overall retina from outer to inner limiting membrane (OLM-ILM) was measured. The thickness of retinal layers in each section was measured in the retina at a distance of 1.5 mm from the center of the optic nerve head.…”

Section: Histological Proceduresmentioning

confidence: 99%

Tacrolimus (FK506) Attenuates Leukocyte Accumulation After Transient Retinal Ischemia

Tsujikawa

Ogura

Hiroshiba

et al. 1998

Stroke

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Background and Purpose-Tacrolimus, an immunosuppressant agent, has been shown to reduce tissue injury and leukocyte accumulation after transient ischemia. This study was designed to evaluate quantitatively the inhibitory effects of tacrolimus on leukocyte rolling and on subsequent leukocyte accumulation in vivo after transient retinal ischemia and the protective effects of tacrolimus on ischemia-induced neural damage. Methods-Retinal ischemia was induced for 60 minutes in anesthetized pigmented rats by temporary ligation of the optic sheath. Tacrolimus was administered at 10 minutes after ischemic induction. At 4, 12, 24, and 48 hours after reperfusion, leukocyte behavior in the retinal microcirculation was evaluated in vivo with acridine orange digital fluorography. After 7 days of reperfusion, ischemia-induced retinal damage was evaluated histologically. Results-Treatment with tacrolimus suppressed leukocyte rolling; the maximum number of rolling leukocytes was reduced by 60.1% at 12 hours after reperfusion (PϽ0.05). In tacrolimus-treated rats, the velocity of rolling leukocytes was significantly faster than in vehicle-treated rats (PϽ0.01). The subsequent leukocyte accumulation was reduced by 61.6% at 24 hours after reperfusion (PϽ0.01). Histological examination demonstrated the protective effect of tacrolimus on ischemia-induced retinal damage, which was more substantial in the inner retina (PϽ0.01). Conclusions-The present study demonstrated the inhibitory effect of tacrolimus on leukocyte rolling and on subsequent leukocyte accumulation and the therapeutic potency to neural injury after transient retinal ischemia. (Stroke.

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“…Various researchers have observed the following numerous histological retinal lesions after ischemia-reperfusion in the rat by temporary ocular hypertonia [6,10,11]: edema and necrosis of the pigmented epithelium, sparseness of nuclei, with pycnosis of inner and outer nuclear layers and reduction of inner and outer plexiform layers.…”

Section: Discussionmentioning

confidence: 99%

“…Several have been proposed: (1) Average thickness of inner retinal layers between the inner bounding membrane and the outer limit of the outer plexiform layer, measured automatically by computer-assisted imaging [6]; (2) the ratio of the thickness of the inner nuclear layer to the total thickness of the retina [11]; (3) the number of nonpycnotic nuclei in the inner nuclear layer [12].…”

Section: Discussionmentioning

confidence: 99%

Scanning Electron Microscopy after Cryofracture of Normal and Ischemic Rat Retinas

Menerath

Droy-Lefaix²,

Doly³

1998

Ophthalmic Res

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The authors described the use of scanning electron microscopy after cryofracture to analyze rat retinas after experimental ischemia-reperfusion sequence. In Sprague-Dawley albino rats, intraocular hypertony by cannulation of anterior chamber was performed for 1 h on one eye. The other eye served as control. After 48 h of reperfusion, retinas were dissected. They were frozen and fractured before ultrastructural analysis by a scanning electron microscope. In the ischemic eyes the thickness of the photoreceptors layer was reduced, through internal disorganization resulting in misalignment of rods. There was swelling of the outer segments, a loss of adhesion between segments and superficial necrosis. Scanning electron microscopy after cryofracture permitted an analysis of the external morphology of retinal cells and intercellular components, especially the outer layers.

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P 351 Monosialoganglioside GM1 reduces ischemia-reperfusion induced injury in the rat retina

Cited by 15 publications

References 0 publications

Protective Effect of Trimetazidine in a Model of Ischemia-Reperfusion in the Rat Retina

Protective Effect of Trimetazidine in a Model of Ischemia-Reperfusion in the Rat Retina

Tacrolimus (FK506) Attenuates Leukocyte Accumulation After Transient Retinal Ischemia

Scanning Electron Microscopy after Cryofracture of Normal and Ischemic Rat Retinas

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