C3a、C5a、MDA、SOD表达在婴幼儿体外循环心肌损伤中作用

Influence of the expressions of C3a,C5a,MDA and SOD on myocardial ischemic and reperfusion injury of cardiopulmonary bypass among infants

目的探讨婴幼儿体外循环(CPB)术后心肌损害机理及预防方法。方法 20例行CPB手术的先天性心脏病患儿分别在CPB转流前、CPB转流结束后20 min(简称术后20 min)、术后2 h、术后6 h、术后12 h测定动脉血浆补体3a(C3a)、补体5a(C5a)、白细胞介素6(IL-6)、肿瘤坏死因子α(TNF-α)、丙二醛(MDA)、超氧化物歧化酶(SOD)、肌酸激酶同工酶(CK-MB)、肌酸激酶(CK)、肌钙蛋白(cTnI)及乳酸脱氢酶(LDH)浓度。结果与CPB转流前比较,术后20 min及2、6、12 h血浆C3a、C5a浓度降低(P<0.05),血浆CK、LDH浓度升高(P<0.05);术后20 min、2 h血浆IL-6浓度逐渐增高(P<0.05),术后6、12 h逐渐下降,但仍高于CPB转流前(P<0.05);血浆TNF-α浓度术后20 min增高(P<0.05),术后2 h开始逐渐下降;血浆CK-MB术后2 h升高(P<0.05),术后6、12 h逐渐下降,但仍高于CPB转流前(P<0.05);术后2 h血浆cTnI升高(P<0.05);血浆MDA浓度术后20 min和2 h降低(P<0.05),术后6 h明显增高(P<0.05),术后12 h降低(P<0.05);血浆SOD浓度术后2、6、12 h明显降低(P<0.05)。结论婴幼儿CPB术后12 h心肌功能明显受损,其机理可能与CPB术后再灌注损伤补体激活及氧自由基释放导致心肌及内皮损伤有关。

Objective To study the mechanism of myocardial ischemic and reperfusion injury and its myocardial protection of cardiopulmonary bypass （ CPB ） among infants. Methods The concentrations of complement 3a （C3a） , complement 5 a （ C5 a）, interleukin-6 （ IL-6 ）, tumor necrosis factor-alpha （ TNF-α）, malonaldehyde （ MDA ）, surperoxide dismntase（ SOD）, creatine kinase MB isoenzyme （CK-MB）, creatine kinase （CK） , troponin （cTnI） and lactic acid dehydrogenase （LDH） were measured before CPB, after CPB 20 min, 2 h, 6 h and 12 h in 20 cases of infants with congenital heart disease. Results Compared with the results before CPB, the levels of C3a and C5a were lower, and the levels of CK and LDH were higher at20 min, 2 h, 6 h and 12 h after CPB（P 〈0.05）. At 20 rain and 2 h after CPB, the levels of IL-6 increased （P 〈0.05）, and at 6 h and 12 h after CPB, the levels of IL-6 decreased, but they were still higher than those before CPB （ P 〈 0.05 ）. The level of TNF-α increased after CPB 20 min （ P 〈 0.05 ）, and decreased after CPB 2 h. The level of CK-MB increased after CPB 2 h （ P 〈 0.05 ） , and decreased after CPB 6 h and 12 h, but it was still higher than that before CPB （P 〈 0.05 ）. The level of cTnI increased after CPB 2 h （P 〈 0.05 ）, and the level of MDA decreased after CPB 20 min and 2 h （ P 〈 0.05 ）, increased significantly after CPB 6 h （ P 〈 0.05 ） , and decreased after CPB 12 h （P 〈0.05 ）. The level of SOD decreased obviously after CPB 2 h, 6 h and 12 h （ P 〈 0.05 ）. Conclusions The myocardial ischemic and reperfusion injury of CPB at 12 h after CRP are serious among infants, and the mechanism of myocardial ischemic and reperfusion injury may be associated with the damages of myocardial and endothelial cells, due to alexin releasing and the increase of oxyradical.