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目的:探讨纳洛酮对心脏骤停后缺血性脑损害的影响。方法:10只犬采用阻断升主动脉和腔奇静脉配合心脏停跳液灌注的方法,造成心脏骤停15分钟后随机分成两组,对照组(5只):常规心肺复苏(CPR);实验组(5只):除常规CPR外,静注纳洛酮0.2mg·kg~(-1)并以0.02mg·kg~(-1)·h~(-1)静滴维持。结果:实验组脑血流量(CBF)、脑灌注压(CPP)在CPR1h、2h、3h明显高于对照组(P<0.05或0.01);CPR3h时实验组脑组织能量物质ATP、ADP、TAN及细胞内酶CK、LDH活性均高于对照组(P<0.01),而LPO低于对照组(P<0.05);实验组脑组织超微结构损害较对照组轻微。结论:纳洛酮通过维持较好的脑内稳态、抑制脂质过氧化、稳定细胞膜、改善能量代谢从而减轻缺血性脑损害。
Objective: To investigate the effect of naloxone on ischemic brain damage after cardiac arrest. Methods: Ten dogs were randomly divided into two groups: control group (CPR), routine cardiopulmonary resuscitation (CPR), blocking the ascending aorta and ventricular arrhythmia with cardioplegia perfusion. Experimental group (n = 5): naloxone was injected intravenously at a dose of 0.02 mg · kg -1 · h -1 intravenously in addition to the conventional CPR. Results: The cerebral blood flow (CBF) and cerebral perfusion pressure (CPP) in the experimental group were significantly higher than those in the control group at 1h, 2h and 3h after CPR (P <0.05 or 0.01) The activity of CK and LDH in the cells were higher than those in the control group (P <0.01), while the LPO was lower than that in the control group (P <0.05). The ultrastructural damage of brain tissue in the experimental group was less than that in the control group. Conclusion: Naloxone can relieve ischemic brain damage by maintaining good brain homeostasis, inhibiting lipid peroxidation, stabilizing cell membrane and improving energy metabolism.