参附注射液对婴幼儿体外循环炎性细胞因子的影响

目的探讨参附注射液对婴幼儿体外循环中细胞因子的影响。方法24例〈3岁的先天性心脏病手术患儿随机均分为两组，参附组于中心静脉穿刺完成后经中心静脉泵注参附注射液1mL／kg（对照组只用生理盐水），于麻醉诱导后即刻、体外循环（CPB）开始时、主动脉阻断时、CPB后20min、CPB结束时及术后6h、24h抽取中心静脉血，采用ELISA法测定血清肿瘤坏死因子-α（TNF—α）、白细胞介素-6（IL-6）含量。结果参附组患儿转窦时间、术后患儿苏醒时间少于对照组（P〈0．05）。麻醉诱导后即刻两组间TNF—α、IL-6水平比较，差异无显著性，CPB后对照组TNF—α、IL-6均升高，CPB20min时达峰值（P〈0．05），术后24h降至术前水平。参附组TNF—α在主动脉阻断时、CPB20min、CPB结束时明显低于对照组（P〈0．05），IL-6在CPB20min时低于对照组（P〈0．05）。结论参附注射液具有缩短转窦时间和术后患儿苏醒时间，并可抑制CPB引起炎性反应的作用。

Effects of Shenfu Injection on Inflammatory Cytokines during Cardiopulmonary Bypass in Infants

OBJECTIVE: To evaluate the effects of Shenfu Injection (SF) on cytokines during cardiopulmonary bypass (CPB) in infants. METHODS: Twenty-four infants with congenital heart disease, aged below three years, were randomly assigned to the control group and the SF group equally. In the SF group, 1 mL/kg of SF was given through center vein pump after center vein puncture being performed, while only normal saline was given instead in the control group. Blood sample was obtained for measurement of serum necrosis factor-alpha (TNF-alpha) and interleukin-6 (IL-6) concentration by ELISA, at various time points in the process, i.e. right after anesthesia induction (T1), beginning of CPB (T2), aortic off-clamping (T3), 20 min after CPB (T4), the end of CPB (T5), and 6 h (T6) and 24 h (T7) after CPB. RESULTS: The time for reverting to sinus heart rhythm and analepsia after CPB was shorter in the SF group than in the control group (P < 0.05). Serum concentration of TNF-a and IL-6 was equal in the two groups at T1; they increased significantly after CPB (P < 0.05), reached the peak value at T4 and reduced to the normal level at T7 in the control group. TNF-alpha concentration was significantly lower at T3, T4 and T5, and IL-6 concentration was lower at T4 in the SF group than that in the control group at corresponding time point (P < 0.05). CONCLUSION: SF could shorten the time for reverting to sinus heart rhythm and analepsia after CPB in infants, and suppress the inflammatory response caused by CPB.