脑缺血后脑微血管ATP酶活性变化

ATPase activity changes of brain microvessels after cerebral ischemia

在建立兔大脑中动脉阻断（ＭＣＡｏ）造成局灶脑缺血模型的基础上，通过不连续密度梯度超速离心分离脑微血管，生化法测定其Ｎａ＋，Ｋ＋－ＡＴＰ酶、Ｃａ２＋，Ｍｇ２＋－ＡＴＰ酶及Ｍｇ２＋－ＡＴＰ酶活性，成巴比妥酸（ＴＢＡ）荧光法测定脑组织丙二醛（ＭＤＡ）含量、黄嘌呤氧化酶法测定脑组织超氧歧化酶（ＳＯＤ）活性。兔随机分为：对照组Ｃ、脑缺血后４小时及２４小时（Ｉ４、Ｉ２４）３组。结果发现Ｉ４组脑微血管Ｎａ＋，Ｋ＋－ＡＴＰ酶活性显著高于对照组（Ｐ＜０．００１），且与脑组织ＭＤＡ之间呈正相关（ｒ＝０．９７Ｏ，Ｐ＜０．００２），而与ＳＯＤ之间呈负相关（ｒ＝－０．８９１，Ｐ＜０．０２；而Ｉ２４组该酶活性则低于对照组。Ｃａ２＋，Ｍｇ２＋－ＡＴＰ酶、Ｍｇ２＋－ＡＴＰ酶在Ｉ４、Ｉ２４组均降低。提示脑缺血后早期脑微血管Ｎａ＋，Ｋ＋－ＡＴＰ酶活性增力。促进早期脑水肿的发生，可能与自由基的刺激有关。

Using the rabbit middle cerebral artery occlu sion (MCAo) model, microvessel segments were isolated from brain by discontinuous density; gra dient centifugation on which the ATPase activities were determined. The content of malondialdehyde (MDA) and the activity of superoxide dismutase (SOD) in brain tissues were determined. Rabbits were randomly divided into three groups: normal and sham-operated control group (c), 4h and 24h after cerebra) ischemisa (I4, I24). We found that in brain microvessels Na+, K+ -ATPase activity signifi cantly increased in I4 group (P<0.001), decreased in I24 group compared to control group and there was positive correlation with MDA in I4 group.The Ca+, Mg2+ -ATPase. Mg2+ -ATPase active ties decteased in both ischemic groups. We propose that in the early cerebral ischemia, the increased activity of brain microvessel's Na+, K+ -ATPase resulted from that oxygen free radicals and exacer bated the early brain edema.