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机构地区:[1]中国医科大学附属第二医院感染科,辽宁沈阳110004
出 处:《中国现代医学杂志》2005年第19期2902-2905,共4页China Journal of Modern Medicine
基 金:国家自然科学基金资助项目(No:30170849)
摘 要:目的建立大鼠内毒素休克模型,取心脏制备光镜及电镜切片,观察心肌细胞超微结构改变,从而探讨感染性休克心脏损伤的可能机制。方法给大鼠1次注射10mg/kg或5mg/kg脂多糖O127:B8,观察平均动脉压及心率的变化。在动物死亡时或观察6h后取心脏制备HE染色切片和电镜切片,镜下观察。结果各组标本HE染色切片光镜下未发现明显病变,电镜下发现内毒素组(无论是10mg/kg还是5mg/kg)均出现线粒体损伤,肌原纤维损伤,闰盘不规则;10mg/kg组损伤程度重于5mg/kg组,还出现充血及血管内皮损伤;处死组出现T管扩张。结论内毒素休克中心脏存在超微结构损伤,而且损伤程度与内毒素剂量相关。[Objective] To investigate the alterations of the ultrastructure of myocardium in endotoxie shock rats in order to inquire the possible mechanisms of cardiac injury in septic shock. [Methods] Endotoxic shock was induced by intravenous infusion of lipopolysaccharide 5 mg/kg or 10 mg/kg, During observation period, we monitored mean arterial pressure(MAP) and heart rate(HR). Take ventrical myocardium at the end of observation and cut into slices for microscopic examination. [Results] There were no obvious changes under light microscope for all groups. Both LPS groups presents mitochondria injury, myofibril injury, irregular intercalated disc under electron microscope. LPS(10 mg/kg) group had congestion and endothelial injury, too. The extent of injury for 10mg/kg group was worse than the 5 mg/kg group. T tubule expansion might be seen in the group of killing in the initial period. [Conclusion] Ultrastructural injury occurs in the heart of endotoxic shock, and the extent of injury is related to the dose of LPS.
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