脓毒症大鼠心功能及氧化应激水平变化

目的观察脓毒症大鼠超声心动图、心肌组织病理学表现及氧化应激水平变化。方法将48只12周龄SD大鼠随机均分为脓毒症24 h组(CLP24 h组)、脓毒症48 h组(CLP48 h组)、假手术组(Sham组)及空白对照组(Blank组)。造模后采用彩色多普勒超声测量各组左心室舒张末期内径(LVEDD)、室间隔舒张末期厚度(IVSD)、左心室后壁舒张末期厚度(LVPWD)、左心室短轴缩短率(LVFS)、左心室射血分数(LVEF)及心率(HR)。对心肌组织行HE及Masson染色,观察心肌组织病理学变化。测定心肌组织超氧化物歧化酶(SOD)、还原型谷胱甘肽(GSH)及丙二醛(MDA)水平,并分析其与LVEF的相关性。结果 4组LVIDD、IVSD、LVFS、LVEF及HR差异均有统计学意义(P均0.01), LVFS、LVEF及HR在Blank组Sham组CLP24 hCLP48 h组。CLP24 h组及48 h组部分心肌细胞肿胀坏死,心肌间隙中胶原纤维明显增多,48 h组更显著。SOD、GSH在Blank组Sham组CLP24 hCLP48 h组,MDA在Blank组Sham组CLP24 h组CLP48 h组。LVEF与SOD、GSH呈正相关(r=0.922 6、0.938 0,P均0.001),与MDA呈负相关(r=-0.929 8,P0.001)。结论脓毒症可引起大鼠心功能异常及心脏结构改变;氧化应激可能是脓毒症致心肌损害的重要机制。

Changes of cardiac function and oxidative stress in sepsis rats

Objective To observe the changes of echocardiography, histopathological manifestations and oxidative stress of myocardium in sepsis rats. Methods Forty-eight 12-week-old SD rats were randomly divided into 4 groups, i.e. cecal ligation and perforation 24 h group (CLP24 h group) and 48 h group (CLP48 h group), sham operation group (Sham group) and Blank group (each n=12). Color Doppler ultrasound was used to measure the left ventricular end-diastolic diameter (LVEDD), interventricular septum thickness at end-diastole (IVSD), left ventricular posterior wall thickness at end-diastole (LVPWD), left ventricular fraction shortening (LVFS), left ventricular ejection fraction (LVEF) and heart rate (HR). HE and Masson staining of myocardial tissues were performed to observe the pathological changes of heart. The levels of superoxide dismutase (SOD), reduced glutathione (GSH) and malondialdehyde (MDA) in myocardial tissues were measured, and the correlations with LVEF were analyzed. Results Statistical differences of LVEDD, IVSD, LVFS, LVEF and HR were found among 4 groups (all P<0.01). LVFS, LVEF and HR in Blank group were all larger than those in Sham group, CLP24 h group and CLP48 h group in turn (all P<0.05). Some myocardial cells in CLP24 h group and CLP48 h groups were swollen and necrotic, while collagen fibers in myocardial space increased significantly and became more obvious in CLP48 h group (all P<0.05). SOD and GSH in Blank group were higher than those in Sham group, CLP24 h group and CLP48 h group in turn, while MDA in Blank group was lower than in Sham group, CLP24 h group and CLP48 h group in turn. LVEF was positively correlated with SOD and GSH (r=0.9226, 0.9380, both P<0.001) and negatively correlated with MDA (r=-0.9298, P<0.001). Conclusion Sepsis can cause abnormalities of function and changes of structure in rat heart. Oxidative stress may be important mechanism for sepsis-induced heart damage.