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目的探讨强化胰岛素治疗对儿童体外循环(CPB)心脏手术炎症介质的影响,及其减轻CPB术后全身炎症反应的机制。方法20例CPB下心脏手术儿童随机分为常规治疗组(RT组,n=10)和强化胰岛素治疗组(IT组,n=10)。IT组患儿术中血糖控制在4.4~10.0 mmol/L(700~1 800 mg/L),术后控制在4.4~8.3 mmol/L(700~1 500 mg/L);RT组患者血糖变化不作处理。分别于术前、麻醉诱导、CPB开始后及CPB结束0,4,12,24和48 h测定两组患儿的血浆胰岛素、白介素-1β(IL-1β)、白介素-6(IL-6)、白介素-10(IL-10)和肿瘤坏死因子α(TNF-α)水平。建立CPB前和CPB结束时在右心耳切口缘取心肌,W estern b lot测定心肌胰岛素受体(InsR)、核转录因子κB(NF-κBp65)表达。结果两组胰岛素水平在CPB开始后上升,于CPB结束时达高峰,随后下降;IT组胰岛素水平从CPB后显著高于RT组(P<0.05,P<0.01)。两组TNF-α和IL-1β、IL-6水平在CPB开始后上升,CPB后3 h达高峰,随后下降;IT组TNF-α和IL-1β、IL-6水平从CPB后开始显著低于RT组(P<0.05,P<0.01)。两组IL-10水平在CPB结束时上升,于CPB 12 h达高峰,随后下降;两组IL-10水平无显著性差异(P>0.05)。CPB后两组InsR表达与CPB前相比均显著增加(P<0.05),强化胰岛素治疗CPB后InsR表达较RT显著增加(P<0.05)。两组CPB后NF-κBp65表达与未干预组相比均显著增加(P<0.05);但CPB后两组间NF-κBp65表达无显著差异。结论强化胰岛素治疗上调胰岛素受体的表达,改善胰岛素抵抗状态,减弱TNF-α和IL-1β、IL-6的表达,起到调节全身炎症反应的作用。
Objective To investigate the effect of intensive insulin therapy on the inflammatory mediators of cardiopulmonary bypass (CPB) during cardiopulmonary bypass (CPB) and its mechanism of reducing the systemic inflammatory response after CPB. Methods Twenty children undergoing cardiac surgery under CPB were randomly divided into routine treatment group (RT group, n = 10) and intensive insulin treatment group (IT group, n = 10). The intraoperative blood glucose was controlled at 4.4-10.0 mmol / L (700-1 800 mg / L) and 4.4-3.3 mmol / L (700-1,500 mg / L) in the IT group. The changes of blood glucose in the RT group No treatment. Plasma insulin, interleukin-1β (IL-1β), interleukin-6 (IL-6) and interleukin-6β (IL-1β) were measured in the two groups at preoperative and postoperative anesthesia, , Interleukin-10 (IL-10) and tumor necrosis factor alpha (TNF-alpha) levels. Myocardium was taken at the margin of the right atrial appendage before CPB and at the end of CPB. The expression of insulin receptor (InsR) and nuclear factor kappa B (NF-κBp65) was determined by Western blot. Results Insulin levels in both groups increased at the beginning of CPB and peaked at the end of CPB, and then decreased. The insulin level in IT group was significantly higher than that in RT group after CPB (P <0.05, P <0.01). The levels of TNF-α, IL-1β and IL-6 in both groups increased at the beginning of CPB and peaked at 3 h after CPB, and then decreased. The levels of TNF-α, IL-1β and IL-6 in IT group were significantly lower after CPB In RT group (P <0.05, P <0.01). The levels of IL-10 in both groups increased at the end of CPB and peaked at 12 hours of CPB, and then decreased. There was no significant difference between the two groups (P> 0.05). InsR expression in both groups increased significantly (P <0.05) before and after CPB, and InsR expression increased significantly (P <0.05) compared with RT after intensive insulin treatment. The expression of NF-κBp65 in CPB group was significantly increased compared with that in the non-intervention group (P <0.05). However, there was no significant difference in the expression of NF-κBp65 between the two groups after CPB. Conclusion Intensive insulin therapy can up-regulate the expression of insulin receptor, improve the insulin resistance and attenuate the expression of TNF-α, IL-1β and IL-6, and play an important role in the regulation of systemic inflammatory response.