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作 者:张素清[1] 杜军保[1] 金红芳[1] 耿彬[2] 李淑葵[3] 张春雨[1] 唐朝枢[2]
机构地区:[1]北京大学第一医院儿科,北京100034 [2]北京大学第一医院北京大学医学部生理与病理生理学系,北京100083 [3]北京大学第一医院检验科,北京100034
出 处:《基础医学与临床》2008年第3期213-216,共4页Basic and Clinical Medicine
基 金:国家自然科学基金(30630031);国家杰出青年科学基金(30425010);国家重点基础性研究项目(2006CB503807);教育部长江学者奖励计划(985-2-087-111)
摘 要:目的观察二氧化硫(SO2)在心肌缺血再灌注损伤中的作用。方法大鼠心脏分为:I/R组,SO2组及天冬氨酸异羟肟酸(HDX)组。采用Langendorff离体心脏灌注模型。MacLab数据采集系统监测离体心脏功能。结果SO2组心功能恢复率明显低于I/R组(P<0.05,P<0.01);HDX组显著高于I/R组(P<0.05,P<0.01)。SO2组冠脉流液中乳酸脱氢酶(LDH)、肌酸激酶(CK)、谷氨酸-草酰乙酸转移酶(GOT)活性、肌红蛋白(Mb)含量及心肌丙二醛(MDA)、共轭双烯键(CD)含量及GOT活性显著高于I/R组(P<0.05,P<0.01);HDX组冠脉流液中上述指标明显低于I/R组(P<0.05,P<0.01)。SO2组心肌还原型谷胱甘肽(GSH)含量明显低于I/R组(P<0.05);HDX组心肌GSH含量显著高于I/R组(P<0.01)。结论SO2参与了大鼠心肌缺血再灌注损伤。增加心肌脂质过氧化及降低心肌还原型谷胱甘肽含量可能与SO2心肌损伤有关。Objective To investigate the effect of SO2 on I/R hearts of rats. Methods Hearts of rat were divided in three groups: I/R group, SO2 group and HDX group. The Langendorff-prepared rat hearts model was used. Heart function was monitored by MacLab system. Results Hearts treated with SO2 showed a decreased recovery rate of heart function as compared with I/R group. HDX group showed an enhanced recovery rate of heart function as compared with I/R group (P 〈 0. 05 or P 〈 0. 01 ). In SO2 group, the lactic dehydrogenase ( LDH), creatine kinase (CK) and glutamic oxaloacetic transaminase (GOT) activities, and myohemoglobin (Mb) content in coronary flow (CF), myocardial malonedialdehyde (MDA), conjugated diene (CD) contents and GOT activities were higher than those of I/R group. Hearts treated with HDX showed decreased LDH, CK and GOT activities, and Mb content in CF , myocardial MDA , CD contents and GOT activities as compared with those of I / R group . In SO2 group, content of GSH decreased as compared with that of I/R group, while in HDX group content of GSH increased as compared with that of I/R group ( P 〈 0. 05 ). Conclusion Endogenous SO2 was involved in the regulation of injury of isolated heart during ischemia and reperfusion. Myocardial injury through SO2 might be related to the increase in lipid peroxide and the decrease in GSH produced by myocardium.
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