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目的:探讨一氧化碳释放分子对心脏骤停并复苏后大鼠神经功能损伤的治疗作用及其机制。方法:建立大鼠窒息法心脏骤停模型,窒息时间约为11分钟,其中心脏骤停时间为6分钟。动物随机分为3组:假手术组;心脏骤停组;心脏骤停复苏后一氧化碳干预组。分别对复苏后的三组大鼠进行神经功能评分、脑海马组织TUNEL凋亡检测,脑ATP含量检测,线粒体呼吸和线粒体膜电位检测分析。结果:大鼠复苏后神经功能评分显著降低并且神经细胞发生大量凋亡,一氧化碳干预组大鼠相比未干预的大鼠,其神经功能评分显著提高,并且其大脑ATP含量、线粒体呼吸及膜电位也显著增强。结论:一氧化碳释放分子通过增强复苏后大鼠脑内线粒体活性而降低大鼠的神经功能损伤。
Objective: To investigate the therapeutic effect and mechanism of carbon monoxide releasing molecule on neurological injury in rats after cardiac arrest and resuscitation. Methods: A cardiac arrest model of rat asphyxia was established. The asphyxiation time was about 11 minutes, and the cardiac arrest time was 6 minutes. The animals were randomly divided into 3 groups: sham operation group; cardiac arrest group; carbon monoxide intervention group after cardiac arrest resuscitation. Three groups of rats after resuscitation were respectively scored for neurological function, TUNEL apoptosis in brain hippocampus, ATP content in brain, mitochondrial respiration and mitochondrial membrane potential. Results: After the rats were resuscitated, the scores of neurological function decreased significantly and the number of apoptotic neurons was significantly increased. Compared with the non-intervention rats, the neurological scores of rats in the carbon monoxide intervention group were significantly increased, and the contents of ATP, mitochondrial respiration and membrane potential Also significantly enhanced. CONCLUSIONS: Carbon monoxide releasing molecules decrease neurological impairment in rats by enhancing mitochondrial activity in the rat brain after resuscitation.