血必净注射液对急性梗阻性黄疸大鼠心肌损伤的保护作用

目的：观察血必净注射液对急性梗阻性黄疸大鼠心肌损伤的保护作用。方法：采用结扎SD大鼠胆总管的方法制作急性梗阻性黄疽动物模型。将54只SD大鼠随机均分为胆总管结扎（BDL）组、胆总管结扎血必净治疗组（XBJ）、假手术组（SO）3组。XBJ组在胆总管结扎后48h开始尾静脉注射血必净注射液，BDL组和SO组同样方法注射等量生理盐水。分别于给药后第3、7、14天各取6只大鼠采样，观察血清胆红素（TBIL）、肌酸激酶同工酶（CK—MB）、内毒素（ET）含量，心肌组织丙二醛（MDA）和超氧化物歧化酶（SOD）含量，以及光镜下观察心肌病理变化。结果：急性胆道梗阻后，血清TBIL、CK—MB、ET水平及心肌组织MDA含量随梗阻时间延长逐渐增高，心肌组织SOD含量减少。XBJ组与同时相BDL组比较，血清TBIL、CK—MB、ET水平及心肌组织MDA含量减少，心肌组织SOD含量增高。光镜下可见随胆道梗阻时间延长，心肌损伤加重，XBJ组与同时相BDL组比较，心肌损伤减轻。结论：血必净注射液对急性胆道梗阻所致心肌损伤有保护作用，作用机制可能与其抗内毒素血症、TNF—α作用及对抗氧自由基有关。

Protection of Xuebijing Injection Against Myocardial Damages Owing to Acute Obstructive Jaundice

Objective：To investigate the protection of Xuebijing injection against myocardial damages owing to acute obstructive jaundice （AOJ）. Methods：The AOJ models in Sprague -Dawley （SD） rats were made by ligating their common bile ducts. The fifty - four SD rats were divided into three groups randomly, namely, bile duct ligation （BDL）, BDL combined with Xuebijing treatment （XBJ）, and sham -operation （SO） groups. The rats in XBJ group were injected with xuebijing via their vena caudalis in 48 hours after their BDL. Same volume of physiological saline was injected into the rats in BDL and SO groups. Six samples from each group were gathered on the 3rd, 7th, 14th days after injeetion. The levels of total bilirubin （TBIL） , MB isoenzyme of creatine kinase （CK-MB） and endotoxin （ET） in sera, contents of malondialdehyde （MDA） and superoxide dismutase （SOD） in myocardium tissues were detected. The pathological changes of myocardium were observed by light microscopy. Results：After acute biliary obstruction, the levels of TBIL, CK-MB and ET in sera and MDA in cardiac muscles were increased, while SOD content gradually decreased increased along with the time prolonging. Compared with the BDL group, the above-mentioned parameters got more close to normal at the same phase; meanwhile, the myocardial damages were relieved in XBJ group. Conclusions：Xuebijing injection produces a marked protection to myocardial damages caused by acute biliary, obstruction. The mechanism may be related to its effects of anti-endotoxemia, TNF-α and oxygen free radical.