窒息心脏骤停后脑的温度对于脑水肿和脑血流的作用

EFFECF OF BRAIN TEMPERATURE ON BRAIN EDEMA AND BLOOD FLOW AFTER ASPHYXIAL CARDIAC ARREST IN RATS

目的；探讨鼠6min窒息心脏骤停后，脑温度变化对脑水肿和脑血流的作用。方法：在浅麻醉和潘蔻罗宁麻痹下，心脏骤停前和后3h使用间歇正压通气。窒息6min后，给肾上腺素和碳酸氢钠并立即开始心肺复苏。激光－多谱勒血流计在皮质连续测定脑血流。在心脏骤停后3h，用碘125标记的白蛋白和湿重与干重的比例来测定脑水肿。自主循环恢复后15min，脑的温度，1组（n＝8）降低到30～31℃，2组（n＝8）保持在37～38℃，3组（n＝8）升高到39～40℃，保持3h，直肠的温度均保持在37～38℃，T检验比较组间资料的差异。结果：在自主循环恢复后1h和2h，1组完全防止了皮质低灌注，2组和3组的皮质脑血流明显低于心脏骤停前。血脑屏障渗透指数，1组（8．9±1．8）明显低于2组（17．1±2．4，P＜0．05）。结论：心脏骤停后，选择性脑低温能增加脑血流和预防脑水肿。

Aim: To investigate the effects of post-ischemic brain temperature changes on brain edema formation and cerebral blood flow after 6 min of asphyxial cardiac arrest in rats. Methods: Under light anesthesia and paralysis with pancuronium, IPPV was used before and to 3 hours after cardiac arrest. After 6 min of asphyxia,epinephrine and bicarbonate were given and CPR instituted. Cerebral blood flow was measured continuously in the cortex using laser-Doppler flowmetry. Brain edema was measured 3 hours after cardiac arrest using I-125 labelled albumin and wet: dry ratio. Fifteen min after ROSC brain temperature was reduced to 30~31 degrees in group 1 (n=8), kept at 37~38 degrees in group 2 (n=8) and increased to 39~40 degrees in group 3 (n=8) which maintained for 3 hours. Rectal temperature was maintained at 37~38 degrees in all groups. Group data were compared with ANOVA and Student's t-test. Results: Selective brain cooling in group 1 completely prevented hypoperfusion at 1 and 2 hours ROSC: whereas CBF was lower than baseline at 1 and 2 hours ROSC in groups 2 and 3. The blood brain barrier permeability index was significantly lower in group 1 (8. 9±1. 8) compared to group 2 (17. ±2. 4,P<0. 05). Conclusion: Selective brain cooling after cardiac arrest increases cerebral blood flow and prevents brain edema in rats.