Ozbay Davut, Ozden Serap, Müftüoğlu Sevda, Kaymaz Figen, Yaylali Volkan, Yildirim Cem, Tatlipinar Sinan
Department of Ophthalmology, Pamukkale University Medical Faculty, Denizli, Turkey.
Can J Ophthalmol. 2004 Dec;39(7):727-32.
A short period of ischemia can induce remarkable tissue resistance to the deleterious effects of subsequent ischemia and reperfusion. We performed a study to investigate the effect of ischemic preconditioning on retinal ischemia-reperfusion injury in rats.
Ten Wistar albino rats were divided into two groups of five animals (10 eyes): one group underwent 5 minutes of ischemic preconditioning (achieved by clamping the common carotid arteries at the time of vertebral artery cauterization), and the other did not (control group). In both groups, the vertebral arteries were occluded bilaterally with an electric needle coagulator under an operating microscope. Forty-eight hours later the rats were reanesthesized, and both common carotid arteries were clamped to interrupt blood flow. The duration of ischemia was 30 minutes. The clamp was then removed to enable reperfusion for 4 hours. The animals were killed by decapitation, and retinal sections were evaluated under light and electron microscopy. The signs of ischemia-reperfusion injury (cellular degeneration, vacuolization between retinal layers, increase in retinal thickness due to edema, mononuclear cell infiltration and apoptotic cell count) were recorded.
Light microscopy of retinal sections from rats in the ischemic preconditioning group showed a well-preserved retinal structure. The mean thickness values (and standard deviation [SD]) for the inner nuclear layer (104.0 microm [2.54 microm] vs. 49.0 microm [ 10.83 microm]) and inner plexiform layer (134.8 microm [10.13 microm] vs. 88.5 microm [17.46 microm]) were significantly higher in the control group than in the preconditioning group (p = 0.009), indicating increased retinal thickness in the former group due to tissue edema resulting from ischemia-reperfusion injury. The mean mononuclear cell count (6.67 [SD 1.97] vs. 2.5 [SD 1.0]) and apoptotic cell count (18.2 [SD 5.7] vs. 5.3 [SD 1.0]) were significantly higher in the control group than in the preconditioning group (p = 0.002), indicating an inhibitory effect of ischemic preconditioning on leukocyte infiltration and apoptotic cell death.
Ischemic preconditioning attenuated ischemia-reperfusion injury in the rat retina.
短时间的缺血可诱导组织对随后的缺血和再灌注的有害影响产生显著抗性。我们开展了一项研究，以调查缺血预处理对大鼠视网膜缺血-再灌注损伤的影响。
将10只Wistar白化大鼠分为两组，每组5只动物（10只眼）：一组进行5分钟的缺血预处理（通过在烧灼椎动脉时夹闭颈总动脉来实现），另一组不进行预处理（对照组）。在两组中，在手术显微镜下用电子针凝血器双侧闭塞椎动脉。48小时后，再次麻醉大鼠，并夹闭双侧颈总动脉以中断血流。缺血持续时间为30分钟。然后松开夹子以实现4小时的再灌注。通过断头处死动物，并在光镜和电镜下评估视网膜切片。记录缺血-再灌注损伤的体征（细胞变性、视网膜层间空泡化、因水肿导致的视网膜厚度增加、单核细胞浸润和凋亡细胞计数）。
缺血预处理组大鼠视网膜切片的光镜检查显示视网膜结构保存良好。对照组内核层（104.0微米[2.54微米]对49.0微米[10.83微米]）和内网状层（134.8微米[10.13微米]对88.5微米[17.46微米]）的平均厚度值（及标准差[SD]）显著高于预处理组（p = 0.009），表明前一组因缺血-再灌注损伤导致组织水肿而使视网膜厚度增加。对照组的平均单核细胞计数（6.67[SD 1.97]对2.5[SD 1.0]）和凋亡细胞计数（18.2[SD 5.7]对5.3[SD 1.0]）显著高于预处理组（p = 0.002），表明缺血预处理对白细胞浸润和凋亡细胞死亡具有抑制作用。
缺血预处理减轻了大鼠视网膜的缺血-再灌注损伤。
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