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大鼠心脏骤停期间不同程度的保护性低温的结局影响

Outcome effects of different protective hypothermia levels during cardiac arrest in rats.

作者信息

Yli-Hankala A, Edmonds H L, Jiang Y D, Higham H E, Zhang P Y

机构信息

Department of Obstetrics and Gynecology, Helsinki University Central Hospital, Finland.

出版信息

Acta Anaesthesiol Scand. 1997 Apr;41(4):511-5. doi: 10.1111/j.1399-6576.1997.tb04733.x.

Abstract

BACKGROUND

Although hypothermia is widely used to protect the brain during cardiac and neurologic surgery, the optimal level of cooling has not been established. This study examined the protective effect of graded levels of surface cooling on cerebral function in rats after complete global cerebral ischemia.

METHODS

Groups of ketamine-anesthetized rats (13 animals in each group) were cooled to cranial temperatures of 34, 30, 27, 24, or 22 degrees C before circulatory arrest. Also a normothermic (37 degrees C) group was tested. After cooling, an 11-min circulatory arrest was produced by atraumatic chest compression. Circulatory arrest was followed by cardiopulmonary resuscitation and rewarming without postischemic intensive care. On the fifth postinsult day, neurologic outcome was scored on a 50-point neurodeficit scale (NDS 0 = normal). The percent of ischemic pyramidal neurons in the CA1 hippocampal region was also determined.

RESULTS

There were no survivors in the normothermic group. Neurologic recovery was enhanced with 30 degrees C cranial temperature, as compared to outcome in the 34 degrees C group. Further cooling did not change outcome. The neurodeficit scales were significantly lower in all other groups compared to the 34 degrees C group on the fifth postinsult day. The percent of ischemic neurons did not change significantly as a function of cooling, but the lowest count appeared at 27 degrees C.

CONCLUSION

In this model, moderate (30 degrees C) cooling improved neurologic outcome. There was no additional benefit from more extreme hypothermia.

摘要

背景

尽管低温疗法在心脏手术和神经外科手术中被广泛用于保护大脑,但最佳的降温水平尚未确定。本研究探讨了分级体表降温对大鼠全脑缺血后脑功能的保护作用。

方法

将氯胺酮麻醉的大鼠分组(每组13只动物),在循环停止前将其冷却至颅骨温度34、30、27、24或22摄氏度。同时设置一个正常体温(37摄氏度)组作为对照。降温后,通过无创胸部按压造成11分钟的循环停止。循环停止后进行心肺复苏和复温,且不进行缺血后重症监护。在损伤后第5天,采用50分神经功能缺损量表(NDS 0 = 正常)对神经功能结局进行评分。同时还测定了海马CA1区缺血锥体神经元的比例。

结果

正常体温组无存活者。与34摄氏度组相比,颅骨温度为30摄氏度时神经功能恢复得到增强。进一步降温并未改变结局。在损伤后第5天,所有其他组的神经功能缺损量表评分均显著低于34摄氏度组。缺血神经元的比例并未随降温而显著变化,但在27摄氏度时数量最少。

结论

在该模型中,适度(30摄氏度)降温可改善神经功能结局。更深度的低温并无额外益处。

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