全脑低灌时脑的乳酸、乳酸脱氢酶、磷酸肌酸激酶的变化及对血或肝中这些参数水平和肠屏障的影响

目的和方法： 阻断小鼠一侧颈总动脉和对侧椎动脉（２Ａ） ，余剩供脑血藉Ｗｉｌｌｉｓ 氏环重分配以模拟近似全脑低灌（ｂｒａｉｎ ｈｙｐｏｐｅｒｆｕｓｉｏｎ ， ＢＨ） 。在全身动脉血压正常情况下研究其意义。结果：在两动脉低灌（ ＢＨ－ ２Ａ） 时，脑静脉血乳酸相对恒定，脑组织乳酸脱氢酶（ＬＤＨ） 不变，磷酸肌酸激酶（ＣＰＫ） 降低，外周血乳酸降低，血糖正常。不变的血糖可在ＢＨ－ ３ Ａ 时升高，认为上述变化是ＢＨ－ ２Ａ 抑制所致，血糖从不变到升高是脱抑制。肝ＬＤＨ 活性降低，ＣＰＫ 不变提示外周血乳酸降低发生在肝外。所有上述变化均可被预先应用６５４ － ２ 所预防。ＢＨ － ２Ａ 和手术操作均可引起近似程度的皮质醇升高，两种应激原的效应差异在皮质醇未见到，却在引起肠源性内毒素（ＥｎＥＴ） 入侵的程度上显示出ＢＨ－２Ａ 的效应较强。结论： 脑低灌对脑ＣＰＫ 活性和外周血乳酸、血糖、肝ＬＤＨ 均有抑制作用，ＢＨ － ２Ａ 是一种应激原可损伤肠屏障导致ＥｎＥＴ 入侵。

The alterations of brain lactate, lactate dehydrogenase, creatine phosphokinase and its influence on these of peripheral blood or liver tissue and entero - barrier during brain hypoperfusion

AIM and METHODS: Mice were subjected to brain hypoperfusion (BH) by occluding unilateral arteria carotis and contralateral arteria vertebro-basilar(BH-2A), which approached to whole brain-hypoperfusion by blood through balencing and redistributing in Willis circle arteries, to study its significance in normal arterial blood pressure condition. RESULTS:In BH-2A group, lactate in cerebral venous blood remained relatively constant, lactate dehydrogenase (LDH) of brain tissue had no changes, creatine phosphokinase (CPK) decreased markedly; peripheral blood: lactate decreased, glucose had no change, while it increased in BH-3A group, all above was caused by the prohibitory effect of BH-2A; glucose increment in BH-3A group is due to glucose escaped inhibition. Liver LDH decreased , CPK had no change, means that the decrement of peripheral blood lactate was not in the liver. All these can be prevented by pretreated with 654-2. Cortisol content had no difference between Sham and BH-2A 90min group,but it increased significantly comparing with the normal. The positive rate of entero genous endotoxin(EnET) in BH-2A 90min group increased markedly than Sham.CONCLUSIONS: BH-2A have prohibitory effect on brain CPK, peripheral blood lactate and liver LDH. BH-2A is a stress factor that can injury the entero-barrier and cause invasion of EnET.