基础医学与临床 ›› 2008, Vol. 28 ›› Issue (3): 213-216.

• 研究论文 • 上一篇    下一篇

二氧化硫对大鼠缺血再灌注心脏的损伤作用

张素清 杜军保 金红芳 耿彬 李淑葵 张春雨 唐朝枢   

  1. 北京大学第一医院 北京大学第一医院儿科 北京大学第一医院儿科 北京大学医学部 生理与病理生理学系 北京大学心血管研究所 北京大学第一医院儿科 北京大学第一医院心血管病研究所
  • 收稿日期:2007-05-18 修回日期:2007-08-22 出版日期:2008-03-25 发布日期:2008-03-25
  • 通讯作者: 杜军保

Injury role of sulfur dioxide on myocardium ischemia and reperfusion rats

Su-qing ZHANG, Jun-bao DU, Hong-fang JIN, Bin GENG, Shu-kui LI, Chun-yu ZHANG, Chao-shu TANG   

  • Received:2007-05-18 Revised:2007-08-22 Online:2008-03-25 Published:2008-03-25
  • Contact: Jun-bao DU,

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(hydroxamate, 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。

关键词: 心脏, 缺血再灌注损伤, 二氧化硫

Abstract: Abstract: Oxidative stress and calcium over loading are thought to be important mechanism of ischemia and reperfusion (I/R) injury and main target of prevention and cure on studies for I/R injury. However, so far, mechanism of I/R injury yet is not completely clear. Sulfur dioxide (SO2) is a common outdoor air pollutant and is associated with day to day changes in hospitalization rates for lung disease. Our group found that SO2 could relax vascular smooth. We presume SO2, especially; endogenous SO2 may have important significance in physiology and pathology in I/R injury. In this a study, we investigated the action of SO2 on I/R hearts of rats. Methods: Hearts of rat was divided in three groups, I/R group; SO2 group; and HDX group. The Langendorff-prepared rat hearts model was used. The heart was under ischemia for 2 hours under hypothermic (40C) subsequent reperfusion/rewarming for 60min. Heart function was monitored by MacLab system for data collection. Results: In SO2 group recovery of heart function(LVP, ±dp/dtmax, HR, CF)decreased compared with that of group of I/R (p<0.05 or p<0.01); In HDX group recovery of heart function(LVP, ±dp/dtmax, HR, CF)increased compared with that of group of I/R (p<0.05 or p<0.01); In SO2 group activity of lactate dehydrogenase (LDH), Creatinekinase (CK), glutamic oxaloacetic transaminase (GOT), and content of myohemoglobin (Mb) in coronary flow (CF); content of Malonedialdehyd (MDA) and conjugated diene (CD), and GOT activity in tissue of cardiac muscle increased compared with I/R group (p<0.05 or p<0.01). In HDX group activity of LDH, CK, GOT, and content of Mb in CF; content of MDA and CD, and GOT activity in tissue of cardiac muscle decreased compared with those of I/R group (p<0.05 or p<0.01). In SO2 group content of glutathione (GSH) decreased compared with I/R group (p<0.05); In HDX group content of GSH increased compared with that of I/R group (p<0.05). In SO2 group content superoxide anion (O2-.), and hydroxyl radical (.OH) were produced by tissue of cardiac muscle, content of hydrogen peroxide (H2O2) and activity of superoxide dimutase (SOD) in tissue of cardiac muscle did not change compared with those of I/R group (p>0.05); In HDX group O2-., .OH were generated by cardiac muscle tissue, content of H2O2 and SOD activity in cardiac muscle tissue did not differ from those of I/R group (p>0.05). Conclusions: (1) endogenous SO2 was involved in isolated heart I/R injury of rat, and this injury was aggravated by exogenesis SO2. (2) Endogenous SO2 produced by tissue possibly increased in isolated heart I/R model of rat. (3) The fact that SO2 damage cardiac muscle tissue was through at least partly through increasing lipid peroxide of cardiac muscle tissue. (4) The fact that SO2 increased lipid peroxide of cardiac muscle tissue was through at least partly through decreasing GSH produced by cardiac muscle.

Key words: heart, ischemia and reperfusion (I/R) injury, sulfur dioxide (SO2)