|Endogenous Sulfur Dioxide Aggravates Myocardial Injury in Isolated Rat Heart With Ischemia and Reperfusion|
|Zhang, Suqing1; Du, Junbao1,2; Jin, Hongfang1; Li, Wei1; Liang, Yinfang1; Geng, Bin3; Li, Shukui4; Zhang, Chunyu1; Tang, Chaoshu2,3|
|关键词||Heart Ischemia and reperfusion (I/R) injury Endogenous sulfur dioxide (SO(2)) Lipid peroxide Reduced glutathione (GSH)|
|WOS标题词||Science & Technology|
|类目[WOS]||Immunology ; Surgery ; Transplantation|
|研究领域[WOS]||Immunology ; Surgery ; Transplantation|
|关键词[WOS]||GAMMA-GLUTAMYLCYSTEINE SYNTHETASE ; FREE-RADICALS ; GLUTATHIONE ; EXPOSURE ; SULFITE ; STRESS ; ORGANS ; DAMAGE ; OXIDE ; MICE|
Background. Ischemia-reperfusion (I/R) injury is an important clinical problem. This article investigated the role Of Sulfur dioxide (SO,) in the regulation of cardiac function and in the pathogenesis of cardiac I/R injury in isolated rat heart.
Methods. Rat hearts isolated on a Langendorff apparatus were divided into control, I/R, I/R+SO(2), and I/R+hydroxamate groups. Hydroxamate is an inhibitor of SO, synthetase. I/R treatment was ischemia for 2 hr in hypothermic solution (4 degrees C), then reperfusion/rewarming (37 degrees C) for 60 min. Cardiac function was monitored by MacLab analog to a digital converter. Determination of sulfite content involved reverse-phase high performance liquid chromatography with fluorescence detection. Myoglobin content of coronary perfusate was determined at 410 run. Myocardial malondialdehyde (MDA) was determined by thiobarbituric acid method, and conjugated diene (CD) was extracted by chloroform. 5,50-Dithiobis-2-nitrobenzoic acid was used to determine glutathione (GSH).
Results. The results showed that I/R treatment. obviously increased myocardial sulfite content, and sulfite content of myocardium was negatively correlated with the recovery rate of left-ventricle developed pressure and positively correlated with the leakage of myoglobin. In postreperfusion, myocardial function recovery was decreased by SO(2). During reperfusion, myocardium-released enzymes, MDA and CD level were increased but myocardial GSH content was depressed with the treatment of SO, donor. Incubation of myocardial tissue with SO(2) significantly increased MDA and CD generation.
Conclusions. Endogenous SO, might be involved in the pathogenesis of myocardial I/R injury, and its mechanism might be associated with an increase in lipid peroxide level and a decrease in GSH generation.
|作者单位||1.Minist Educ Mol Cardiol, Hlth Sci Ctr, Key Lab, Beijing, Peoples R China|
2.Peking Univ, Hosp 1, Dept Pediat, Beijing 100871, Peoples R China
3.Peking Univ, Hlth Sci Ctr, Dept Physiol & Pathophysiol, Beijing 100871, Peoples R China
4.Peking Univ, Hosp 1, Dept Clin Lab, Beijing 100871, Peoples R China
|Zhang, Suqing,Du, Junbao,Jin, Hongfang,et al. Endogenous Sulfur Dioxide Aggravates Myocardial Injury in Isolated Rat Heart With Ischemia and Reperfusion[J]. TRANSPLANTATION,2009,87(4):517-524.|
|APA||Zhang, Suqing.,Du, Junbao.,Jin, Hongfang.,Li, Wei.,Liang, Yinfang.,...&Tang, Chaoshu.(2009).Endogenous Sulfur Dioxide Aggravates Myocardial Injury in Isolated Rat Heart With Ischemia and Reperfusion.TRANSPLANTATION,87(4),517-524.|
|MLA||Zhang, Suqing,et al."Endogenous Sulfur Dioxide Aggravates Myocardial Injury in Isolated Rat Heart With Ischemia and Reperfusion".TRANSPLANTATION 87.4(2009):517-524.|
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