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目的 研究缺氧缺血时脑内组织型纤溶酶原激活物 (TPA)与脑微血管基膜的细胞外基质降解的相关性。 方法 一日龄 SD大白鼠分为空白对照组、假手术组和 3个缺氧缺血时间不同的实验组 (n=12 )。每组取 4例脑测 TPA活性 ,取 8例脑用抗 型胶原、层粘连蛋白和纤维粘连蛋白抗体标记。 结果 在 3个实验组中以缺氧缺血组的 TPA活性最高 ,而后随着复氧时间的增加而下降 (P<0 .0 1)。实验组的 型胶原、层粘连蛋白和纤维粘连蛋白阳性染色平均单位面积比对照组 (空白组、假手术组 )小 (P<0 .0 1)。实验组阳性产物呈不连续线状的微血管数比对照组多 (P<0 .0 1)。缺氧缺血组鼠脑严重充血水肿 ,脑重比对照组显著增加。 结论 缺氧缺血可以激发新生大白鼠脑内 TPA活性增高 ,然后通过一系列酶促反应 ,使微血管基膜的细胞外基质成分— 型胶原、层粘连蛋白和纤维粘连蛋白等降解 ,血脑屏障受损 ,微血管渗透性增加 ,发生脑水肿 ,甚至脑出血。
Objective To investigate the relationship between the expression of tissue-type plasminogen activator (TPA) and the degradation of extracellular matrix in brain microvascular basement membrane during hypoxic-ischemic brain damage. Methods One-day-old SD rats were divided into blank control group, sham operation group and three experimental groups with different hypoxic-ischemic time (n = 12). The brain activity of TPA was measured in 4 cases in each group, and 8 cases were labeled with anti-collagen, laminin and fibronectin antibodies. Results The TPA activity of hypoxic-ischemic group was the highest in three experimental groups, and then decreased with the increase of reoxygenation time (P <0.01). The average unit area of positive staining of collagen, laminin and fibronectin in the experimental group was smaller than that in the control group (blank group, sham operation group) (P <0.01). Experimental group positive products were discontinuous linear microvascular number than the control group (P <0.01). Hypoxic ischemic rat brain congestion and edema, brain weight increased significantly than the control group. Conclusion Hypoxia-ischemia can activate TPA activity in the brain of neonatal rats, then through a series of enzymatic reactions, the extracellular matrix components of the vascular basement membrane-type collagen, laminin and fibronectin degradation, blood-brain barrier Impairment, increased capillary permeability, cerebral edema, and even cerebral hemorrhage.