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目的:探讨脂氧素A4对新西兰兔心脏骤停心肺复苏(CPR)后血流动力学、心肌坏死面积、心肌细胞结构(光镜和电镜)、血清心肌酶水平的影响。方法:健康新西兰大白兔16只,雌雄不限,随机分为空白组(假手术组)(n=4)、对照组(CPR+乙醇组)(n=6)和实验组(CPR+脂氧素组)(n=6)。所有实验动物耳缘静脉麻醉,气管切开行气管插管,左侧颈总动脉、右颈内静脉及股动脉置管。对照组和实验组动物,夹闭气管插管5-9min后引起动物窒息,诱导心脏骤停3min后,开始胸外按压,机械通气(纯氧),静脉注射200μg/kg的肾上腺素,同时实验组静脉给予脂氧素A4(1.5μg/kg)乙醇溶液,对照组给予等体积的2%乙醇溶液。监测自主循环恢复(ROSC)4h的血流动力学指标,于ROSC后6h股动脉取血检测肌酸激酶同工酶(CK-MB),然后处死取心脏标本,测量心肌坏死面积,检测光镜HE染色、电镜下心肌结构变化,观察脂氧素对上述指标的影响。结果:对照组和实验组复苏后反映心室收缩功能和舒张功能的dp/dtmax、-dp/dtmax以及平均动脉压均显著低于复苏前(P<0.01),但实验组复苏后的收缩、舒张功能和平均动脉压的改善要明显优于对照组(P<0.01);实验组较对照组血清CK-MB值显著降低(P<0.01),左心室坏死范围减小(P<0.05),心光镜和电镜下显示心肌结构损伤减轻,未见炎性细胞浸润。结论:脂氧素A4可抑制心肌内炎症反应,减轻心脏骤停兔心肺复苏后的心肌结构损害,同时改善心室收缩、舒张功能和血压,从而改善心功能不全。
Objective: To investigate the effects of lipoxin A4 on hemodynamics, myocardial necrosis area, myocardial cell structure (light and electron microscopy) and serum myocardial enzymes in New Zealand rabbits after cardiac arrest and cardiopulmonary resuscitation (CPR). Methods: Totally 16 New Zealand white rabbits were randomly divided into blank group (sham operation group) (n = 4), control group (CPR + ethanol group) (n = 6) and experimental group ) (n = 6). All experimental animals were anesthetized with auricle vein, endotracheal intubation, left common carotid artery, right internal jugular vein and femoral artery were cannulated. In the control group and experimental group, animals were asphyxiated 5-9 minutes after tracheal intubation, and cardiac arrest was induced for 3 minutes. Thoracic compression, mechanical ventilation (pure oxygen) and intravenous injection of 200 μg / kg of epinephrine were performed simultaneously Groups were given liposomal A4 (1.5μg / kg) ethanol intravenously and control group was given an equal volume of 2% ethanol solution. The hemodynamic indexes of spontaneous circulation recovery (ROSC) for 4 hours were measured. The creatine kinase isoenzyme (CK-MB) was measured at 6 hours after ROSC in the femoral artery. The heart specimens were sacrificed and the area of myocardial necrosis was measured. HE staining, changes in myocardial structure under electron microscope to observe the impact of lipoxin on the above indicators. Results: The dp / dtmax, -dp / dtmax and mean arterial pressure of the control group and experimental group after resuscitation were significantly lower than those before resuscitation (P <0.01). However, after the resuscitation, the contractile and diastolic Function and mean arterial pressure were significantly better than those in the control group (P <0.01). Serum CK-MB was significantly lower in the experimental group than in the control group (P <0.01), and the range of left ventricular necrosis was decreased (P <0.05) Light and electron microscopy showed myocardial structural damage reduced, no inflammatory cell infiltration. Conclusion: Lipoxin A4 can inhibit the myocardial inflammatory reaction, relieve cardiac structural damage after cardioversion in rabbits with cardiac arrest, and improve ventricular systolic and diastolic function and blood pressure, thus improving cardiac insufficiency.