氯胺酮对先天性心脏病患者体外循环心肌诱导型一氧化氮合酶mRNA表达的影响

目的观察氯胺酮预处理对先天陛心脏病患者体外循环诱导心肌缺血再灌注损伤时诱导型一氧化氮合酶（iNOS）mRNA表达的影响。方法先天性心脏病房间隔缺损或室间隔缺损患者36例，随机分为三组（n=12）：对照组（C组）和氯胺酮干预组（K，组和K2组）。在劈胸骨时、主动脉插管时和主动脉开放前5min，K1、K2组分别静脉注射氯胺酮0．5mg／kg和1．0mg／kg，C组注射等量0．9％NaCl溶液。于上腔静脉插管时（T1）、主动脉阻断后30min（T2）和主动脉开放后30min（T3）取适量心肌组织，应用一步法实时荧光定量RT-PCR技术检测心肌中iNOS mRNA的表达量。结果与T1比较，三组T2和T3iNOS mRNA均升高（P〈0．01）；与C组（2．85±0．48、4．49±0．86）比较，K1、K2组T2和T3iNOS mRNA均显著降低（2．33±0．31、3．76±0．61和1．92±0．12、3．12±0．39）；K2组与K1组比较，T2和T3iNOS mRNA均降低（P〈0．05）。结论氯胺酮预处理能显著降低心肌iNOS mRNA的表达量，减少血浆心肌酶的漏出，且呈剂量依赖性。

Effects of ketamine pretreated on the expression of myocardium induced nitric oxide synthase mRNA in congenital heart disease patients undergoing cardiopulmonary bypass

Objective To investigate the effects of ketamine preconditioning on the expression of induced nitric oxide synthase （iNOS） mRNA after myocardial ischemia-repeffusion injury induced by cardiopulmonary bypass （CPB） in patients with congenital heart disease （CHD）. Methods Thirty-six patients with atrial or ventricular septal defect were randomly allocated to 3 groups （n = 12）： control group and ketamine preconditioning group （K1 group, K2 group）. Ketamine 0.5 mg/kg and 1.0 mg/kg, were injected at the time of sternum splitted, aorta intubated and before 5 minutes of aorta clamped off intravenously. Collected the myoeardium at the time of superior vena eava intubated （T1）, 30 minutes after aorta clamped on （T2） and 30 minutes after aorta clamped off （T3）. Detected the value of iNOS mRNA in myoeardium by one-step real time fluorescence quantitative RT-PCR. Results The levels of iNOS mRNA were significantly increased at T2 and T3 as compared with T1 in the three groups, and were significantly lower both in K1 group （2.33 ± 0.31, 3.76 ± 0.61 ） and K2 group （ 1.92 ± 0.12, 3.12 ± 0.39） than those in control group （2.85 ± 0.48,4.49 ± 0.86） （P 〈 0.01 or 〈 0.05）. Furthermore, they were lower in K2 group than those in K1 group （P 〈 0.05）. Conclusion Ketamine can significantly decrease iNOS mRNA in myoeardium, and decrease the plasma marker of cardiac muscle injury, it Shows dose dependent.