EFFECT OF SELENIUM AND GLUTATHIONE PEROXIDASE IN MYOCARDIAL PROTECTION IN INFANTS

本研究旨在探讨婴幼儿心肌保护不如成人的原因。硒是人体必需的微量元素，是谷胱甘肽过氧化物酶(GSHPx)的组成部分。实验分为三组，第一组为出生后8-12天的幼鼠，第二组为饲喂低硒饲料的成年大鼠(缺硒大鼠)，第三组为饲喂正常饲料的成年大鼠(对照组)。幼年大鼠(3.81~0.81g/g蛋白质)和低硒大鼠(2.06~1.69g/g蛋白质)的血清Se水平显著低于对照组(7.32~2.94g/g蛋白质)(p&lt；0.01)。仔鼠血清GSHPx活性(22.7±3.5U/g蛋白)和低硒大鼠血清GSHPx活性(24.6±22.2U/g蛋白)显著低于对照组(179.6±12.0U/g蛋白)(P<0.01)；心脏中GHSPx活性分别为0.48±0.11U/mg蛋白和0.34±0.03U/mg蛋白，显著低于对照组(0.80±0.06U/mg蛋白)(P<0.01)。而仔鼠心脏硒含量是缺硒大鼠和对照组大鼠的5.1倍。低硒大鼠的脂质过氧化水平(19.6±3.7 nM/mg蛋白)显著高于对照组(8.96±4.4 nM/mg蛋白)(P<0.01)。测定低硒大鼠和正常大鼠离体心的机械功能。低硒大鼠在4℃停跳63分钟后再灌流30分钟后，主动脉压、心输出量和LV dp/dt显著降低(p&lt；0.05)。提示Se代谢紊乱所致的GSHPx降低可能是再灌注期脂质过氧化程度增加，心肌保护不良的原因之一。

This study was undertaken to ascertain the reason why the myocardial protection was inferior in the infants to that in adults. The essential trace element, Selenium(Se), is a integral part of glutathione peroxidase(GSHPx). The rats were divided into three groups, first, infant rats 8-12 days after birth, Second, mature rats fed se-deficient diet (Se-deficient rats), third, mature rats fed normal diet (control rats). Serum Se level in infant rats (3.81 0.81 g/g protein) and in Se-deficient rats (2.06 1.69 g/g protein) was significantly lower than that in control rats (7.32 2.94 g/g protein)(p<0.01). Serum GSHPx activity in infant rats (22.7+3.5 U/g protein) and in Se-deficient rats (24.6+22.2 U/g protein) was significantly lower than that incontrol rats (179.6 12.0 U/g protein)(p<0.01).GHSPx activity in the heart in infant rats (0.48 0.11 U/mg protein)and in Se-defivient rats (0.34 0.03 U/mg protein) was significantly lower than that in control rats (0.80 0.06 u/mg protein) (p<0.01). However, Se lein the heart of infant rats was 5.1 times more than that of Se-deficient rats and control rats. Lipid peroxide level in Se-deficient rats (19.6 3.7 nM/mg protein) was significantly more than that incontrol rats (8.96 4.4 nM/mg protein)(&<0.01). Cardiac mechanical function was determined in isolated working heart in Se-deficient and control rats. After 30 minutes' perfusion following 63 minutes' cardiac arrest at 4 C, aortic pressure, cardiac output and LV dp/dt were significantly lower in Se-deficient rats (p<0.05). These results suggest that low GSHPx caused by disturbance of Se metabolism may more lipid peroxidation during reperfusion and poor myocardial protection in infants.