PENTOBARBITAL PROTECTION FROM CEREBRAL INFARCTION WITHOUT SUPPRESSION OF EDEMA
PENTOBARBITAL PROTECTION FROM CEREBRAL INFARCTION WITHOUT SUPPRESSION OF EDEMA
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DOI：
10.1161/01.str.13.5.623
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发表时间：
1982-01-01
期刊：
影响因子：
8.3
通讯作者：
NEWFIELD, P
中科院分区：
文献类型：
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作者：
HOFF, JT;NISHIMURA, M;NEWFIELD, P
通过观察猫左大脑中动脉（LMCA）急性永久性闭塞72小时后水肿形成的详细情况，研究巴比妥酸盐对局灶性脑梗死的保护机制。术后观察神经功能、气体交换、生命体征及颅内压（ICP）。牺牲后测量梗死面积和脑水肿。只有在闭塞前给予戊巴比妥并持续24小时后，梗死面积才会减小。尽管梗死范围得到抑制，但水肿的形成并未受到抑制。尽管戊巴比妥足以减少梗死面积，但大多数猫在闭塞后仍出现脑卒中的临床证据和颅内压升高。尽管进行了强化心肺支持，但ICP升高仍是导致大多数过早死亡的原因。戊巴比妥治疗的猫缺血半球的水和电解质变化在关闭后72小时内持续发展，表明药物延迟了水肿的消退。显然，戊巴比妥可以减小猫的梗死面积并缩短缺血性水肿的预期时间，但该药物对动脉闭塞后发生的水肿的严重程度几乎没有影响。
The mechanism of barbiturate protection from focal cerebral infarction was studied in cats by examining in detail edema formation 72 h after acute, permanent occlusion of the left middle cerebral artery (LMCA). Neurological function, gas exchange, vital signs and intracranial pressure (ICP) were observed during the postocclusion period. Infarct size and cerebral edema were measured after sacrifice. Infarct size was reduced only when pentobarbital was given before occlusion and continued for 24 h. Edema formation was not suppressed even though the extent of infarction was. Clinical evidence of stroke developed and ICP rose in most cats after occlusion despite the presence of pentobarbital sufficient to reduce infarct size. Elevated ICP accounted for most premature deaths despite intensive cardiopulmonary support. Water and electrolyte changes in the ischemic hemisphere continued to develop throughout the 72-h postocclusion period in pentobarbital-treated cats, suggesting that resolution of edema was delayed by the drug. Apparently, pentobarbital reduces infarct size and attenuates the expected time course of ischemic edema in cats, but the drug has little effect on the severity of edema that develops after arterial occlusion.