To investigate the role of oxidative stress in myocardial injury induced by high-voltage electrical burns in rats and the intervention effect of N-acetylcysteine (NAC).

A total of 220 male SD rats were randomly divided into sham injury group (n=60), electrical burn group (n=60), saline group (n=50) and NAC group (n=50). The observation time was 0 h, 8 h, 24 h, 48 h, 72 h and 1 week after injury, with 10 rats in each group. The experimental high-voltage electrical shock system was used to establish a rat model of high-voltage electrical burn with a voltage of 3 kV and a shock of 3 s, with the left forelimb and right hind limb of rats as the inlet and outlet of current, respectively. Rats in the saline group were intraperitoneally injected with normal saline 1 mL/kg. Rats in NAC group were intraperitoneally injected with 10%NAC 1 mL/kg (100 mg/kg). Myocardial tissue was collected at regular intervals in each group, and superoxide dismutase (SOD) activity, the content of malondialdehyde (MDA) and myeloperoxidase (MPO) in myocardial homogenate supernatant were detected. The morphological changes of myocardium were observed under light microscope.

Compared with those in sham injury group, the SOD activity, MDA content and MPO content of myocardial tissue in electrical burn group increased (all P<0.001). The activity of SOD in myocardial tissue of rats in electrical burn group was higher than that in sham injury group at post-injury 48 h(P=0.037). The content of MDA in myocardial tissue of rats in electrical burn group was higher than that in sham injury group at post-injury 8 h(P=0.009), 24 h(P=0.006), 48 h(P< 0.001), and 72 h(P<0.001). The content of MPO in myocardial tissue of rats in electrical burn group was higher than that in sham injury group at post-injury 8 h(P<0.001), 24 h(P<0.001), 48 h (P=0.002), and 72 h(P=0.008). The SOD activity increased at first and then decreased within 1 week after electroacupuncture, and reached the peak at 48 hours. The content of MDA firstly increased and then decreased, and reached the peak at 48 hours. The content of MPO decreased gradually. Compared with the electrical burn group at each time point, the SOD activity, MDA and MPO content in the saline group and NAC group showed no statistical significance (all P>0.05). Compared with sham injury group, intercalated discs disappeared, horizontal lines blurred, cell edema, inflammatory infiltration, muscle bundle separation and interstitial focal hemorrhage were observed in electrical injury group within 0-48 hours. The edema and inflammatory infiltration of cardiomyocytes were the most obvious at 48 hours. Myocardial tissue edema and inflammation were gradually reduced during 48 h-1 week. Compared with the electrical burn group, there was no significant improvement in myocardial injury in the saline and NAC groups.

High-voltage electrical burns can cause myocardial injury by increasing myocardial oxidative stress level in rats. NAC has no significant effect on SOD activity, MDA content, MPO content in myocardial tissue of rats with high-voltage electrical burns and myocardial injury at 48 h post burn.