纳洛酮对猫局灶性脑缺血的影响。

H Kobayashi, H Ide, M Hayashi
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引用次数: 6

摘要

我们研究了单次注射纳洛酮(5mg /kg,静脉注射)对大脑中动脉(MCA)经眶闭塞引起的脑缺血猫的影响。测定脑血流量(CBF),根据动静脉(A-V)氧差测定脑代谢耗氧量(cmoro2)。6只猫在闭塞后30分钟用纳洛酮治疗,8只猫在闭塞后2小时用纳洛酮治疗。在6只对照动物中,纳洛酮使平均动脉血压(MABP)、CBF和CMRO2持续30分钟升高10-15%。MCA闭塞使同侧MCA区域的CBF减少70-75%,对侧半球减少15%。在两个治疗组中,纳洛酮使缺血区CBF增加3.5% -6%,对侧半球CBF增加10% -22%,其程度与对照动物相同。A-V氧差无明显变化,两组非缺血区cmor2的估计升高与对照组相似。这些影响是短暂的,持续15-60分钟。我们得出结论,纳洛酮引起脑代谢的短暂增加等于或超过相应的CBF增加。因此,纳洛酮对脑缺血的治疗并无益处,反而可能是有害的。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Effect of naloxone on focal cerebral ischemia in cats.

We have examined the effects of a single injection of naloxone (5 mg/kg, i.v.) in cats with cerebral ischemia produced by transorbital occlusion of the middle cerebral artery (MCA). Cerebral blood flow (CBF) was measured and the cerebral metabolic rate of oxygen consumption (CMRO2) was estimated based on measurements of arteriovenous (A-V) oxygen difference. Six cats were treated with naloxone 30 minutes after occlusion and 8 were treated 2 hours after occlusion. In 6 control animals, naloxone produced a 10-15% increase in mean arterial blood pressure (MABP), CBF and CMRO2 lasting 30 minutes. MCA occlusion reduced CBF by 70-75% in the ipsilateral MCA territory and by 15% in the contralateral hemisphere. Naloxone increased CBF by 3.5-6% in the ischemic region and 10-22% in the contralateral hemisphere in both treatment groups to the same extent as seen in control animals. There was no significant change in A-V oxygen difference and the estimated increase in CMRO2 of non-ischemic regions of both treatment groups was similar to that of control animals. These effects were transient and lasted 15-60 minutes. We have concluded that naloxone caused a transient increase in cerebral metabolism which equals or exceeds the corresponding increase in CBF. Therefore, naloxone would not be beneficial, and may be detrimental in the treatment of cerebral ischemia.

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