缺血缺氧时新生大鼠脑微血管基膜细胞外基质与脑细胞线粒体钙的变化

CHANGES OF MICROVASCULAR BASEMENT MEMBRANE AND EXTRACELLULAR MATRIX AND CHANGES OF MITOCHONDRIAL CALCIUM IN BRAIN OF NEONATAL RATS ON ISCHEMIA HYPOXIA

本文用６０ 只新生大鼠随机分为空白对照组、假手术对照组、缺血缺氧组、复氧２４ ｈ 组和复氧４８ ｈ 组。对每组中的４ 例大脑用抗Ⅳ型胶原抗体和抗层粘连蛋白抗体进行免疫组织化学反应；每组中的８ 例测定脑细胞线粒体钙浓度。用方差分析ＳｔｕｄｅｎＮｅｗ ｍ ｅｎＫｅｕｌｓ 法检验所得数值的差异显著性，Ｐ＜ ０．０５。缺血缺氧组、复氧２４ ｈ 组和复氧４８ ｈ 组Ⅳ型胶原和层粘连蛋白阳性反应平均单位面积分别比两对照组者小；三个实验组阳性反应呈不连续线状的微血管数比两对照组者多；同时三个实验组阳性反应呈连续线状的微血管数比两对照组者少。三个实验组之间的阳性反应呈不连续线状的微血管数或呈连续线状的微血管数也都存在着显著性差异。缺血缺氧组脑细胞线粒体钙含量比两对照组者高，缺血缺氧后复氧２４ ｈ 组继续升高，复氧４８ ｈ 组的脑细胞线粒体钙含量却下降。缺血缺氧可导致新生脑细胞线粒体的钙离子增多，并可能激活细胞外的蛋白酶，溶解微血管的基膜成分－ Ⅳ型胶原和层粘连蛋白等，损伤血脑屏障，渗透性增高，发生脑水肿。如果能够及时给予合理的治疗和处理，则应该可以得到一定程度的恢复。

Ischemia hypoxia encephalopathy is a severe injury to neonates. 60 neonatal SD rats were randomly divided into 5 groups: 2 control groups and 3 experiment groups. 8 brains per group were treated with antibodies against collagen Ⅳ and laminin, and the concentration of mitochondrial calcium in 4 brains per group were measured. Average areas of positive immunoreaction production and microvessel counts of continuous linear reaction staining of two antibodies in ischemia hypoxia, 24 h after ischemia hypoxia and 48 h after ischemia hypoxia groups were less than that of two control groups (P<0.05). However microvessel counts of discontinuous linear immunoreaction products of 3 experiment groups were more than that of two control groups(P<0.05). Calcium concentration in ischemia hypoxia group was higher than in two control groups, and the calcium concentration in 24 hours after ischemia hypoxia group was the highest, while 48 hours after ischemia hypoxia group it was lowered(P<0.05). On ischemia hypoxia the concentration of mitochondrial calcium goes up, proteases was activated; it dissolved basement membrane of microvessels, injured the blood brain barrier and promoted osmosis. Then edema occurred. If ischemia hypoxia is treated in time, the process may be prevented according to our study. (Figures 1～4 on plate 39)