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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。
OBJECTIVE: To block one side of the common carotid artery and the contralateral vertebral artery (2A), and the rest for cerebral blood circulation by Willis’s ring redistribution to simulate the approximate brain hypoperfusion (BH). Study its meaning in the context of normal systemic arterial pressure. Results: Cerebral venous blood was relatively constant with lactate dehydrogenase (LDH), phosphorylated creatine kinase (CPK) decreased, peripheral blood lactate decreased, and blood glucose was normal during low arterial infusion (BH- 2A). Immobilized blood sugar can be elevated in BH- 3 A, that the above changes are caused by inhibition of BH- 2A, blood glucose does not change to rise is off inhibition. Liver LDH activity decreased, unchanged CPK prompted peripheral blood lactate occurred in the extrahepatic. All of the above changes can be prevented by prior application of 654-2. Both BH - 2A and surgical procedures induced similar increases in cortisol, and the differences in the effects of the two stressors were not seen in cortisol but showed BH at a level that induced enterogenic endotoxin (EnET) invasion -2A strong effect. Conclusion: Cerebral hypoperfusion can inhibit the activity of CPK and lactate, blood glucose and LDH of liver in a dose - dependent manner. BH - 2A is a stressor that can damage the intestinal barrier and lead to EnET invasion.