中文摘要：

目的评价δ受体在吗啡预处理减轻慢性心力衰竭大鼠心肌细胞缺氧复氧损伤中的作用。方法健康成年雄性SD大鼠，体重220—250g，尾静脉注射阿霉素2mg／kg，每周1次，共6次，末次注射后2周取心脏，分离、培养心肌细胞，采用随机数字表法，将其随机分为5组（n=8）：对照组（C组）、缺氧复氧组（H／R组）、吗啡预处理组（MPC组）、吗啡预处理＋阿片受体拮抗剂纳洛酮组（MPC＋Naloxone组）和吗啡预处理＋δ受体拮抗剂纳曲吲哚组（MPC＋Natrindole组）。c组正常培养，余组细胞行缺氧3h，复氧1h。MPC组于缺氧前即刻行吗啡预处理。MPC＋Naloxone组和MPC＋Natrindole组于吗啡预处理前10min时分别加入纳洛酮（终浓度10μmol／L）和纳曲吲哚（终浓度μmol／L）。于复氧1h时采用MTT法测定心肌细胞活力，检测乳酸脱氢酶（LDH）和肌酸激酶（CK）活性，Hoechst33234染色法检测心肌细胞凋亡情况，计算细胞凋亡率。结果与C组比较，H／R组、MPC＋Naloxone组和MPC＋Natrindole组心肌细胞活力降低，LDH、CK活性和心肌细胞凋亡率升高（P〈0．05）；与H／R组比较，MPC组心肌细胞活力升高，LDH、CK活性和心肌细胞凋亡率降低（P〈0．05），MPC＋Naloxone组和MPC＋Natrindole组上述各指标差异无统计学意义（P〉0．05）。结论吗啡预处理通过激活8受体抑制慢性心力衰竭大鼠心肌细胞缺氧复氧损伤。

英文摘要：

Objective To evaluate the role of δ receptor in reduction of hypoxia-reoxygenation （H/R） injury to cardiomyocytes by morphine preconditioning in rats with chronic heart failure. Methods Adult male Sprauge-Dawley rats weighing 220-250 g were used in the study. Chronic heart failure was induced by injection of adriamycin 2 mg/kg via the tail vein once a week for 6 weeks. Their hearts were removed 2 weeks after the last injection and the cardiomyocytes were isolated and cultured. The cells were randomly divided into 5 groups （ n = 8 each） ： control group （group C） ; H/R group; morphine preconditioning group （group MPC） ; morphine preconditioning ＋ naloxone （opioid receptor antagonist） group （group MPC ＋ Naloxone） ; morphine pieconditioning ＋ naltrindole （δ receptor antagonist） group （MPC ＋ Naltrindole group）. The cells were cultured in normal culture atmosphere in group C and were exposed in hypoxic air for 3 h followed by 1 h reoxygenation in the other groups. Mor- phine preconditioning was performed immediately before hypoxia in group MPC. Naloxone and naltrindole were added before morphine preconditioning in groups MPC ＋ Naloxone and MPC ＋ Natrindole respectively. At 1 h of reoxygenation, the cell viability （by MTT assay）, activities of lactate dehydrogenase （LDH） and creatine kinase （CK）, and cell apoptosis were detected. The apoptotic rate was calculated. Results The cell viability was significantly lower, and the activities of LDH and CK and apoptotic rate were significantly higher in groups H/R, MPC ＋ Naloxone and MPC ＋ Natrindole than in group C （ P 〈 0.05）. The cell viability was significantly higher, and the activities of LDH and CK and apoptotic rate were significantly lower in group MPC than in group H/R （ P 〈 0.05 ）. Conclusion Morphine preconditioning reduces H/R injury to cardiomyocytes through activating δ receptor in rats with chronic heart failure.