【摘要】 目的观察缺血再灌注时大鼠视网膜分泌组织型纤溶酶原激活剂(tissue-type plasminogen activator,TPA)和 TPA 抑制物(plasminogen activator inhibitor,PAI)的变化,并探讨其意义。方法采用提高眼压法造成视网膜缺血后,恢复眼压形成血流再灌注。实验分5组:正常对照组、缺血1 h 再灌注1 h 组、缺血1 h 再灌注2 h组、缺血2 h 再灌注1 h 组和缺血2 h 再灌注2 h 组,每组各取10例测试视网膜组织 TPA 和 PAI 的活性。结果缺血再灌注后,大鼠视网膜组织 TPA 的活性随缺血和再灌注时间的延长而升高(P<0.01);PAI 的活性无显著性变化(P>0.05);TPA/PAI 的比值随缺血和再灌注时间的延长而增大(P<0.01)。结论缺血再灌注引起视网膜组织 TPA 活性的升高,TPA 和 PAI 动态平衡受破坏,是导致视网膜组织水肿和损伤的因素之一。更多还原

【Abstract】 Purpose To observe the changes of activity of tissue-type plasminogen activator(TPA)and plasminogen activator inhibitor(PAI)in the retinas of rats following iscbemia and reperfusion.Methods The intraocular pressure(IOP) was increased to occlude retinal biood vessels to induce retinal ischemia,then IOP was lowered to allow reperfusion.The animals were divided a control group and 4 isschemia-reperfusion groups to detect the activity of TPA and PAI.Results The activity of TPA increased after ischemia-reperfusion(P<0.01),the activity of PAI did not change(P>0.05),the proportion of TPA/PAI increased after ischemia-reperfusion(P<0.01).Conclusion Iscbemia and reperfusion can stimulate the rising of activity of TPA,destroy the balance between TPA and PAI.They may be one of factors that induced retinal edema and damage after ischemia-reperfusion.更多还原