探讨氧化应激在大鼠高压电烧伤心肌损伤中的作用及N-乙酰半胱氨酸(NAC)的干预效果。

采用随机数字表法将雄性SD大鼠220只分配至假伤组(60只)、电伤组(60只)、盐水组(50只)及NAC组(50只)，观测时相为伤后0 h、8 h、24 h、48 h、72 h、1周，相应观测时相点各10只。采用实验高压电击系统，以大鼠左前肢及右后肢分别为电流入口和出口，制作电压3 kV、电击3 s的大鼠高压电烧伤模型。盐水组大鼠腹腔注射生理盐水1 mL/kg；NAC组大鼠腹腔注射10%NAC 1 mL/kg(100 mg/kg)。每组按时相采集心肌组织，检测心肌匀浆上清液超氧化物歧化酶(SOD)活性、丙二醛(MDA)水平、髓过氧化物酶(MPO)水平。光镜下观察心肌组织形态学改变。

与假伤组比较，电伤组大鼠心肌组织总体SOD活性、MDA水平、MPO水平均增高(均P<0.001)。电伤组SOD活性在伤后48 h高于假伤组(P＝0.037)，MDA水平在伤后8 h(P＝0.009)、24 h(P＝0.006)、48 h(P<0.001)、72 h(P<0.001)均高于假伤组，MPO水平在伤后8 h(P<0.001)、24 h(P<0.001)、48 h(P＝0.002)、72 h(P＝0.008)均高于假伤组。电后1周内，SOD活性先增高后降低，48 h达峰值；MDA先增高后降低，48 h达峰值；MPO逐渐降低。与电伤组各时相相比，盐水组及NAC组SOD活性、MDA水平、MPO水平差异均无统计学意义(均P>0.05)。与假伤组比较，电伤组0～48 h内心肌细胞之间闰盘消失，横纹模糊，细胞水肿，炎性浸润，肌束分离，间质灶性出血；48 h心肌细胞水肿及炎性浸润最明显；48 h～1周心肌组织水肿、炎症等症状逐渐减轻。与电伤组比较，盐水组和NAC组心肌损伤均无明显改善。

高压电烧伤通过提高大鼠心肌氧化应激水平导致心肌损伤。NAC对大鼠高压电烧伤后心肌组织SOD活性、MDA水平、MPO水平及伤后48 h的心肌损伤干预效果不明显。

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.