目的：对大鼠全身炎症反应综合征(SIRS)模型心肌亚细胞结构、能量代谢的变化进行研究，以期进一步了解心肌能量代谢改变在SIRS向多器官功能障碍综合征发生发展过程中的作用。方法：Wistar大鼠随机分为SIRS-A组(内毒素注射后1 h)、SIRS-B组(内毒素注射后3 h)及对照组(Con)。高效液相色谱法测定各组大鼠心肌ATP，ADP和AMP的含量。大鼠心肌细胞进行透射电镜检查。结果：①SIRS-A组ATP，ADP及AMP含量分别为(1.51±0.39)×10-1，(3.22±0.59)×10-1和(2.17±0.56)×10-1mmol/g；SIRS-B组为(1.31±0.53)×10-1，(2.75±0.74)×10-1，(1.88±0.57)×10-1mmol/g；对照组为(2.57±0.82)×10-1，(5.75±0.69)×10-1，(5.35±0.76)×10-1mmol/g，3组ATP，ADP和AMP含量差异有显著性(P<0.05 或 0.01)。SIRS-A组，SIRS-B组的ATP，ADP和AMP含量低于对照组(P<0.05)；SIRS-B组与SIRS-A组之间ATP，ADP和AMP含量差异无显著性(P>0.05)。②透射电镜观察可见SIRS大鼠心肌细胞线粒体排列紊乱，空泡变性，肌纤维水肿。结论：能量代谢障碍和线粒体功能结构的改变等在SIRS发展为MODS过程中起到了重要的作用。

OBJECTIVE: To study the changes of the myocardial cellular structure and energy metabolism and to explore the effects of myocardial energy metabolic disorders on the development into the multiple organ dysfunction syndrome (MODS) in systemic inflammatory response (SIRS) rats. METHODS: The SIRS rat model was created by injecting high dose endotoxin (20 mg/kg). The contents of ATP, ADP and AMP were measured with the method of HPLC in the myocardium of the SIRS A group rats (1 hour after injections of endotoxin), the SIRS B group rats (3 hours after injections of endotoxin) and the control group rats (no endotoxin was given). The pathological changes in all the SIRS rats were studied with the electron microscope. RESULTS: The contents of ATP, ADP and AMP in the SIRS A group rats [( 1.51 ± 0.39 )×10 -1 ,( 3.22 ± 0.59 )×10 -1 and ( 2.17 ± 0.56 )×10 -1 mmol/g] and the SIRS B group rats [( 1.31 ± 0.53 )×10 -1 ,( 2.75 ± 0.74 )×10 -1 and ( 1.88 ± 0.57 )×10 -1 mmol/g] were lower than those in the control group rats [( 2.57 ± 0.82 )×10 -1 ,( 5.75 ± 0.69 )×10 -1 and ( 5.35 ± 0.76 )×10 -1 mmol/g](P< 0.05 ). No significant difference in the ATP, ADP and AMP contents was found between the SIRS A group rats and SIRS B group rats. Under the electron microscope, the mitochondria in myocardium cells revealed structural disorders with vacuolar degeneration and edematous myocardial fibers in all the SIRS rats. CONCLUSIONS: Energy metabolism disorders and mitochondria dysfunctions of the myocardium may play an important role in the development of SIRS.