| Objectives To investigate the protective effect of intravitreal injection dexamethasoneand triamcinolone acetonide for retina ischemia-reperfusion injury(RIRI) of rabbit in orderto provide the experimental basis for the treatment of RIRI using them and explore newtreatment approach for the clinical treatment of diseases with RIRI pathological process.Methods81healthy pure Japanese rabbits (male, weighing2.0～2.5kg) were randomlydivided into three groups. Group1was normal control group, containing5rabbits, withoutany treatment. The other two groups were experimental injury groups, containing76rabbits, wherein the right eyes belonged to injury control group, the left ones belonged toinjury treatment group. The rabbits of experimental injury groups received retina ischemia-reperfusion injury by the method of anterior chamber perfusion to elevate intraocularpressure.100ul mixed liquor of dexamethasone and triamcinolone acetonide (volume ratio1:1) immediately were injected into vitreous of right eyes after injury. Left eyes wereinjected into equal sodium lactate ringer’s injection. The experimental injury groups didfundus photography and fluorescein angiography at ischemia instant and6h,12h,24h,48h,72h,1w after reperfusion with4rabbits alive at each time point. Similarly, the normalcontrol group was randomly chosen2rabbits to do that. The eye tissues were takenimmediately after death at1h,6h,12h,24h,48h,72h,1w after reperfusion for HE stainingand immunohistochemical detection of wt-p53and Caspase-3proteins using6rabbits ateach time point. Similarly, the normal control group was randomly chosen3rabbits to dothat. In addition, other6rabbits repeatedly did optical coherence tomography examinationbefore modeling and at1h,6h,12h,24h,48h,72h,1w after modeling and accuratelymeasured retinal thickness. All the datas were statisticed with the SPSS17.0software.Results1fundus photography: Normal retina of rabbit is jacinth, and the retinal vesselsarranged well. After ischemia, retina is pale with vascular occlusion. After reperfusion,the color of retina was dark red with dilated blood vessels, and retina edema wasgradually developed with white cotton wool exudates, which were most serious in rabbitsat24hour point. Injury treatment group compared with injury control group at each timepoint, the degree of retina edema and white cotton wool exudates was reduced.2FFAinspection: There was no fluorescein leakage in normal retina. After ischemia,fluorescein retained in the optic disc, and retinal blood vessels had absent fluoresceinfilling. After reperfusion, the blood vessels of optic disc and retina restored filling withfluorescein leakage and non-perfusion area. The leakage volume of fluorescein was themost at24hour point. Injury treatment group compared with injury control group at eachtime point, the degree of vessel occlusion and the leakage volume of fluorescein wasreduced.3OCT inspection: The retinal thickness of injury control group and injurytreatment group at1week after modeling, respectively, compared with that before injury were thin, the differences were statistically significant (P<0.05); The retinal thickness ofinjury control group was thinner than that in injury treatment group at1week aftermodeling, the difference was statistically significant (P<0.05). From the injury begainingto24hour after injury segment,; From24hour to1week, treatment factors, time factors,treatment factors and time factors interactions had also statistically significant differences(P>0.05).4HE dyeing: The three layers of cells from normal rabbit retina showed a cleardemarcation and arranged neatly and tightly. After reperfusion, retina edema wasgradually developed with gradually increasing cell gap and karyopyknosis dispersedlydistributed among ganglion cell layer(GCL) and inner nuclear layer(INL), which weremost serious in rabbits at24hour point, then retinal edema gradually reduced, and thenumber of retinal ganglion cells(RGC) and INL cells also gradually reduced at48and72hour points. Retinal edema disappeared completely, RGC and INL cells significantlyreduced, and inner plexiform layer and nerve fiber layer atrophy and thin at1week point.Pathological changes of retina in injury treatment group at each time point was consistentwith that in injury control group, but lighter than that in injury control group.5wt-p53and Caspase-3protein immunohistochemical staining: We did not detect brown positivecells in normal retina. After reperfusion, the positive cells appeared in GCL of injurycontrol group by chance at1hour point. Positive cells began to increase at6hour point,mainly in GCL. The number of positive cells was further increased, mainly in GCL, andINL also had a small amount of positive cells at12hour point. Positive cells reached apeak at24hour point, Besides GCL, INL also see part of positive cells.48hour still sawa lot of positive cells.72hour had markedly decreased;1week basically saw no positivecells. The change trends of positive cells number of wt-p53and Caspase-3in injurytreatment group were consistent with that in injury control group, but positive cellsnumber of wt-p53and Caspase-3in injury treatment group was obviously less than thatin injury control group at6～72hour section (P<0.05). The difference between twoadjacent time points in injury control group and injury treatment group was statisticallysignificant(P<0.05). The positive cells number both reached a peak at24hour point.Conclusions1Retinal edema is one of the expression of RIRI and apoptosis may be theend result of RIRI.2Dexamethasone combined with triamcinolone acetonide protect RIRIby inhibiting apoptosis and reducing retinal edema.3OCT examination has a very highvalue in assessing the extent and treatment effect of RIRI. |
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