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目的:观察和探讨葛根素(puerarin)预处理对体外循环(cardiopulmonary bypass,CPB)下小儿先天性心脏病心脏直视手术中心肌缺血再灌注损伤的防治作用及炎性反应机制。方法:选择先心病小儿20例,随机分为两组。一组为葛根素预处理观察组(观察组),一组为生理盐水对照组(对照组)。观察组于CPB前静脉输注葛根素4mg/kg,对照组输注等量生理盐水。分别于T1:CPB前(基础值);T2:主动脉开放后1h;T3:主动脉开放后2h;T4:主动脉开放后4h采集患儿全血4次,4ml/次。采用电化学发光法测定各时点血清心肌特异性肌钙蛋白T(specific myocardialtroponin T,c-TNT)浓度;采用酶联免疫吸附实验(ELISA)测定各时点致炎性细胞因子白介素-6(IL-6)、白介素-8(IL-8)、肿瘤坏死因子α(TNF-α)。结果:观察组各时点血清c-TNT浓度均低于对照组;观察组各时点血清致炎性细胞因子IL-6、IL-8、TNF-α浓度也均低于对照组。结论:葛根素预处理可明显减轻先心病小儿开心手术中心肌缺血/再灌注损伤;抑制血清致炎性细胞因子IL-6、IL-8、TNF-α的表达可能是其心肌保护作用的炎性反应机制。
Objective: To observe and discuss the preventive and therapeutic effects of puerarin preconditioning on myocardial ischemia-reperfusion injury in children with congenital heart disease under cardiopulmonary bypass (CPB) and its mechanism of inflammatory reaction. Methods: 20 cases of children with congenital heart disease were randomly divided into two groups. A group of puerarin pretreatment observation group (observation group), a group of saline control group (control group). The observation group received 4 mg / kg puerarin intravenously before CPB, and the control group received the same volume of saline. Respectively before T1: CPB (basic value); T2: 1h after aortic opening; T3: 2h after aortic opening; T4: 4h after complete aortic opening 4h, 4ml / time. The concentration of myocardial specific Troponin T (c-TNT) at each time point was measured by electrochemiluminescence method. The levels of inflammatory cytokines interleukin-6 IL-6), interleukin-8 (IL-8) and tumor necrosis factor alpha (TNF-alpha). Results: Serum levels of c-TNT in the observation group were lower than those in the control group at each time point. Serum levels of IL-6, IL-8 and TNF-α in the observation group were also lower than those in the control group at each time point. CONCLUSION: Puerarin preconditioning can significantly reduce myocardial ischemia / reperfusion injury in children with congenital heart disease (CHD). Inhibition of serum proinflammatory cytokines IL-6, IL-8 and TNF-α may be their cardioprotective effects Inflammatory reaction mechanism.