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目的:明确窒息性心脏骤停(cardiac arrest, CA)后的早期是否就存在缺血性心肌挛缩。方法:建立窒息及室颤诱导的大鼠CA模型，31只雄性Wistar大鼠随机（随机数字法）分为空白对照组、窒息组和室颤组。记录诱发CA过程中的心电图与血压；于CA 0 min时行血气分析检测；于CA 0、2、4、6和8 min分别测量大鼠心脏的长度和宽度；于CA 0和8 min时分别检测心肌三磷酸腺苷（ATP）含量。结果:窒息组诱发CA所用时间长于室颤组[（237±20 ）s n vs （3±1）s，n P<0.05]；窒息组大鼠在CA 0 min已发生严重的低氧血症、二氧化碳潴留及酸中毒，而室颤组大鼠血气检测各项指标基本正常；窒息组大鼠CA后心脏长度及宽度逐渐缩小，CA 6 min左右心肌挛缩达到极限，而室颤组大鼠心脏形态在CA后8 min内无显著变化；CA 0 min时窒息组心肌ATP含量已显著下降(n P0.05)。n 结论:窒息性CA早期即发生心肌挛缩，可能与窒息阶段ATP大量消耗有关。“,”Objective:To investigate the characteristics of ischemic myocardial contracture after asphyxia-induced cardiac arrest (CA).Methods:Asphyxia and ventricular fibrillation (VF) induced cardiac arrest model was established. Thirty-one male Wistar rats were randomly(random number) assigned to the sham, asphyxia and VF groups. Electrocardiogram and blood pressure during CA stage were recorded. Arterial blood was drawn for blood gas analysis at 0 min after CA. The length and width of the heart were measured at 0,2,4,6 and 8 min after CA. The myocardial ATP contents were measured at 0 and 8 min after CA.Results:Compared with the VF group, the time of CA induction was longer in the asphyxia group[ (237±20 ) s n vs (3±1) s, n P<0.05]. At 0 min after CA, severe hypoxemia, carbon dioxide retention and acidosis had occurred in the asphyxia group, while these indexes in the VF group were basically normal. The length and width of the heart in the asphyxia group decreased gradually after CA, the myocardial contracture reached the limit around 6 min after CA, while the cardiac morphology of the VF group did not change significantly during the observation period of 8 min after CA. Myocardial ATP content in the asphyxia group decreased significantly at 0 min after CA (n P0.05).n Conclusions:Myocardial contracture occurrs in the early stage of asphyxia CA, which may be related to ATP consumption in the asphyxia stage.