不同剂量脂多糖对缺血再灌注大鼠心肌功能损害的实验研究  

Effects of different LPS doses on ischemia/reperfusion-induced cardiac injury in rats

作　　者：秦东泽[1] 张涌[1] 郭林静[1] 王志斌[1] 范国昌[2] 韩清华[3] 

机构地区：[1]山西医科大学第一医院心胸外科,太原030001 [2]美国辛辛那提大学 [3]山西医科大学第一医院心内科,太原030001

出　　处：《临床心血管病杂志》2017年第4期371-375,共5页Journal of Clinical Cardiology

基　　金：山西省科技发展计划(社会发展)项目(No:20130313016-12)

摘　　要：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 explore the effect of lipopolysaccharide（LPS）in heart function in rats with myocardial ischemic reperfusion.Method：Rats were pretreated with incremental doses of LPS or normal saline in order to establishing sepsis model in rat.Myocardial ischemia reperfusion was established by occluding left anterior descending artery for 40 minute.STNFαR was additionally used to block the effects of LPS.Result：dp/dt during systole decreased from 4831±213mmHg/s to 2265±114mmHg/s.-dp/dt decreased from 4119±179mmHg/s to 2056±109mmHg/s.Pretreatment with low doses of LPS（〈1μg）had no effect on±dp/dt,However in higher concentrations LPS suppressed both contractility and diastole function.Cardiac troponin I level increased to 9.6±2.5ng/dl following ischemia and continued to rise with higher doses of LPS.Blocking TNF-αdid not improve the myocardial contractility and diastole after ischemia,but it reduced myocardial injury from additional deleterious effects of LPS.Conclusion：Lower doses of LPS have no deleterious effect on myocardial function,whereas higher doses of LPS cause cardiac dysfunction and increase extent of injury.

关 键 词：脂多糖LPS 心肌缺血再灌注 肿瘤坏死因子-Α 

分 类 号：R541.4[医药卫生—心血管疾病]