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目的:探讨脂多糖(LPS)对缺血再灌注大鼠心肌功能的影响。方法:应用不同剂量的LPS腹腔注射建立大鼠败血症模型,通过对大鼠心脏左前降支阻塞40min建立心肌缺血再灌注损伤模型。STNFaR注射阻断LPS对心肌的效应。结果:心肌收缩功能指标dp/dt在缺血期从(4 831±213)mmHg/s降至(2 265±114)mmHg/s,心肌舒张功能指标-dp/dt由(4 119±179)mmHg/s降至(2 056±109)mmHg/s。低剂量LPS(<1μg)对缺血心肌的收缩功能dp/dt和舒张功能-dp/dt没有影响,高浓度的LPS能够抑制心肌收缩和舒张功能。心肌缺血后血清肌钙蛋白I浓度升至(9.6±2.5)ng/dl,伴随着LPS注射浓度增加而升高。阻断肿瘤坏死因子-α(TNF-α)效应后并不能改善缺血心肌收缩和舒张功能,但能减轻LPS所致心肌细胞损伤。结论:低剂量的LPS对缺血再灌注大鼠心肌功能没有明显影响,而高剂量LPS导致心功能功能障碍和心肌损伤加重。
Objective: To investigate the effect of lipopolysaccharide (LPS) on myocardial function in ischemia-reperfusion rats. Methods: A rat model of sepsis was established by intraperitoneal injection of LPS at different doses. The model of myocardial ischemia-reperfusion injury was established by occlusion of the left anterior descending artery in rats for 40 minutes. STNFaR injection blocks the effects of LPS on myocardium. Results: The dp / dt of myocardial systolic function was decreased from (4831 ± 213) mmHg / s to (2665 ± 114) mmHg / s in ischemic period, and the myocardial diastolic function index-dp / dt was (4 119 ± 179) mmHg / s to (2 056 ± 109) mmHg / s. Low dose LPS (<1μg) had no effect on dp / dt and diastolic function-dp / dt of ischemic myocardium. High concentration of LPS could inhibit myocardial contractile and diastolic function. Serum cardiac troponin I concentration increased to (9.6 ± 2.5) ng / dl after myocardial ischemia, with an increase in LPS injection concentration. Blockade of tumor necrosis factor-α (TNF-α) effect does not improve ischemic myocardial contractile and diastolic function, but can reduce LPS-induced cardiomyocyte injury. CONCLUSION: Low-dose LPS has no significant effect on myocardial function in rats with ischemia-reperfusion, whereas high-dose LPS leads to worsening cardiac dysfunction and myocardial injury.