[Myocardial oxidative stress injury and myocardial ultrastructure in septic rats]

To investigate the mechanism of myocardial injury in septic rats by cecal ligation and puncture.

Fifty-four male Sprague-Dawley (SD) rats were randomly divided into 3 groups: normal group (n=6), sham group (n=24), sepsis group (n=24). Cecal ligation and puncture (CLP) was adopted to reproduce animal models of sepsis. The contents of cardiac troponin I (cTnI) and nitric oxide (NO) in serum and the activities of superoxide dismutase (SOD) and malondialdehyde (MDA) in myocardium were detected in each group 3, 6, 12, 24 hours after the operation (with 6 rats at each time point). The changes of myocardial pathomorphology were observed by HE staining under a microscope. The ultrastructural changes of myocardial cells were observed by the electron microscopy.

The levels of serum cTnI and NO in the sepsis group were much higher than those in the sham group and the normal group. At the same time, the activity of MDA in myocardium in the sepsis group was also significantly higher than that in the other two groups. While the activity of SOD was obviously lower. Besides, ultrastructural changes in sepsis ones included myocardial cell edema, inflammatory cell infiltration, interstitial angiectasis and hyperemia and visible focal myocardial necrosis. Myocardial cell injury was more serious in sepsis rats compared with the other two groups. Electron microscopy showed different degrees of disorganized myofibrils, widened intercalated disc gap, decreased mitochondrial cristae and vacuolation of myocardium in sepsis group.

The myocardial cell injury is due to oxidative stress injury in septic rats. As the disease progresses, the myocardial ultrastructure damage becomes worse gradually.