
自体冷血停跳液对婴幼儿心肌保护机制的研究
Myocardial protection of cold autoblood cardioplegia in infants with congenital heart disease
[摘要]目的:研究婴幼儿心内直视手术灌注不同停跳液心肌细胞丙二醛(MDA)和超氧化物歧化酶(SOD)的变化,探讨自体冷血停跳液对婴幼儿心肌保护的作用机制。方法:30例非紫绀型先天性心脏病婴幼儿(体重≤8kg),随机分为晶体液组、冷血组和自体冷血停跳液组,每组10例。分别于心脏停跳前、复跳后取右心耳心肌,检测心肌MDA和SOD含量。术中记录复跳时间、自动复跳率和室颤发生率。术后监测心脏指数(CI),正性肌力药物依赖情况。结果:术前3组MDA分别为(0.87±0.14)、(0.88±0.11)、(0.86±0.15)nmol/mg prot;SOD分别为(61.3±3.4)、(69.2±3.1)、(64.4±4.2)U/g,差异无显著性(P>0.05);同组术后与术前比较,MDA明显升高,分别为(3.12±0.21)、(2.93±0.27)、(1.67±0.15)nmol/mg prot,SOD明显降低(42.6±2.3)、(44.6±3.1)、(57.7±2.1)U/g,差异有显著性(P<0.05或P<0.01);术后自体冷血组与晶体液组、冷血组冷血比较,MDA含量降低,SOD含量升高,复跳时间缩短,正性肌力药物依赖性降低,CI升高,差异均有显著性(P<0.05或P<0.01);晶体液组与冷血组比较,复跳时间、正性肌力药物依赖性及CI差异有显著性(P<0.05或P<0.01)。结论:自体冷血停跳液对婴幼儿心内直视手术心肌保护主要作用机制是降低心肌细胞氧自由基的产生。[中国当代儿科杂志,2009,11(8):638-640]
OBJECTIVE: To study the effects of cold autoblood cardioplegia on oxygen free radicals in the myocardium in infants who underwent cardiopulmonary bypass and to explore the possible mechanism of myocardial protection of autoblood cardioplegia. METHODS: Thirty infants with acyanotic congenital heat disease (CHD) (weight≤8 kg) were randomized to receive cold crystalloid, cold blood or cold autoblood cardioplegia (n=10 each group) during cardiopulmonary bypass. The biopsy samples were taken from the right atrium just before heart arrest and after heart self-recovery for the measurement of malonaldehyde (MDA) and superoxide dismutase (SOD) contents. The time and the rate of the heart self-recovery to sinus rhythm, and the incidence of ventricular fibrillation were recorded during operation. The cardiac index (CI) and the dependence of positive inotropic drugs were monitored after operation. RESULTS: Before the operation, there were no significant differences in myocardial MDA (0.87±0.14, 0.88±0.11 and 0.86±0.15 nmol/mg prot, respectively) and SOD contents (61.3±3.4, 69.2±3.1 and 64.4±4.2 U/g, respectively) among the crystalloid, the blood and the autoblood cardioplegia groups. After operation, the myocardial MDA content increased (3.12±0.21, 2.93±0.27 and 1.67±0.15 nmol/mg prot, respectively) and SOD content (42.6±2.3, 44.6±3.1 and 57.7±2.1 U/g, respectively) decreased significantly in the three groups (P<0.05 or 0.01). The autoblood cardioplegia group had lower myocardial MDA content and higher SOD content than the crystalloid and the blood cardioplegia groups (P<0.05). The time of heart self-recovery was shortened and the dependence of positive inotropic drugs were reduced in the autoblood cardioplegia group compared with the crystalloid and the blood cardioplegia groups (P<0.05). Post-operational CI in the autoblood cardioplegia group was significantly higher than that in the blood and the crystalloid cardioplegia groups. There were significant differences in the time of heart self-recovery, the dependence of positive inotropic drugs and the CI between the blood and the crystalloid cardioplegia groups (P<0.05 or 0.01). CONCLUSIONS: Cold autoblood cardioplegia reduces oxygen free radicals in the myocardium, thus providing myocardial protections in infants undergoing cardiopulmonary bypass.[Chin J Contemp Pediatr, 2009, 11 (8):638-640]
自体冷血停跳液 / 氧自由基 / 心肌保护 / 体外循环 / 婴幼儿
autoblood cardioplegia / Oxygen free radical / Myocardial protection / Cardiopulmonary bypass / Infant
[1]董礼文,都欣毅,杨勇,叶芃. 体外循环中应用中低温含血停跳液诱导停跳的心肌保护作用[J]. 浙江临床医学, 2003, 5(12):895-896.
[2]Kaminski KA, Bonda TA, Korecki J, Musial WJ. Oxidative stress and neutrophil activation-the two keystones of ischemia/reperfusion injury [J]. Int J Cardiol, 2002, 86(1):41-59.
[3]Tabet F, Savoia C, Schiffrin EL, Touyz RM. Differential calcium regulation by hydrogen peroxide and superoxide in vascular smooth muscle cells from spontaneously hypertensive rats[J]. J Cardiovasc Pharmacol, 2004, 44(2):200-208.
[4]Hoffman JW Jr, Gilbert TB, Poston RS, Silldorff EP. Myocardial reperfusion injury: etiology, mechanism, and therapies[J]. J Extra Corpor Technol, 2004, 36(4):391-411.
[5]Belboul A, Roberts D, B-rjesson R, Johnsson J. Oxygen free radical generation in healthy blood donors and cardiac patients: the protective effect of allopurinol[J]. Perfusion, 2001, 16(1):59-65.
[6]Nordlie MA, Wold LE, Simkhovich BZ, Sesti C, Kloner RA. Molecular aspects of ischemic heart disease: ischemia/reperfusion-induced genetic changes and potential applications of gene and RNA interference therapy[J]. J Cardiovase Pharmacol Ther, 2006, 11(1):17-30.
[7]Chen YF, Lin YT. Comparison of blood cardioplegia to electrolyte cardioplegia on the effectiveness of preservation of right atrial myocardium: mitochondrial morphometric study[J]. Ann Thorac Sury, 1985, 39(2):134-138.
[8]Boyle EM Jr, Pohlman TH, Johnson MC, Verrier ED. Endothelial cell injury in cardiovascular surgery: the systemic inflammatory response[J]. Ann Thorac Surg, 1997, 63(1):277-284.
[9]Toyoda Y, Yamaguchi M, Yoshimura N, Oka S, Okita Y. Cardioprotective effects and the mechanisms of terminal warm blood cardioplegia in pediatric cardiac surgery[J]. J Thorac Cardiovasc Surg, 2003, 125(6):1242-1251.
[10]吴歆, 王斌,顾熊飞.人红细胞保护蛋白对羟基自由基的清除作用[J]. 中国生化药物杂志, 2004, 25(5):297-299.