我们的网站为什么显示成这样?

可能因为您的浏览器不支持样式,您可以更新您的浏览器到最新版本,以获取对此功能的支持,访问下面的网站,获取关于浏览器的信息:

|本期目录/Table of Contents|

内源性H2S在大鼠骨骼肌缺血/再灌注所致心肌损伤中的变化及意义

《心脏杂志》[ISSN:1009-7236/CN:61-1268/R]

期数:
2009年第1期
页码:
6-10
栏目:
基础研究
出版日期:
2009-02-28

文章信息/Info

Title:
Change and significance of endogenous H2S during myocardial injury caused by ischemia reperfusion of rat skeletal muscle
作者:
陈雯1刘莉2张颖1齐迎春1张海峰1耿彬3谢晓华1
1.解放军总医院南楼综合外一科,北京 100853;2.解放军306医院心内科,北京100101; 3.北京大学医学部生理系心血管研究室,北京100034
Author(s):
CHEN Wen1 LIU Li2 ZHANG Ying1 QI Ying-Chun1 ZHANG Hai-Feng1 GENG Bin3 XIE Xiao-Hua1
1.Department of Geriatric General Surgery, PLA General Hospital, Beijing 100853, China; 2.Department of Cardiology, PLA 306 Hospital, Beijing 100853, China; 3.Institute of Cardiovascular Diseases, First Hospital, Peking University, Beijing 100034, China
关键词:
骨骼肌缺血/再灌注心肌损伤硫化氢大鼠
Keywords:
skeletal muscle ischemia/reperfusion myocardial injury hydrogen sulfide rat
分类号:
R542.2
DOI:
-
文献标识码:
A
摘要:
目的 研究内源性血浆硫化氢(H2S)/心肌胱硫醚-γ-裂解酶(CSE)体系在骨骼肌缺血/再灌注所致心肌损伤中的变化及作用。方法 雄性Wistar大鼠62只,应用止血带结扎构建大鼠双下肢缺血/再灌注模型。按照缺血及再灌注不同时间点随机分为9组:①正常对照组(C组,8只);②缺血2 h组(I2组,4只);③缺血4 h组(I4组,8只);④再灌注0.5 h组(R0.5组,8只);⑤再灌注2 h组(R2组,8只);⑥再灌注4 h组(R4组,8只);⑦再灌注6 h组(R6组,8只);⑧再灌注12 h组(R12组,4只);⑨再灌注24 h组(R24组,6只)。各再灌注组均为缺血4 h。观察各组大鼠心肌病理改变、血浆H2S、肌酸激酶同工酶(CK-MB)、肌钙蛋白T(TnT)水平的变化及心肌CSE活性的变化。结果 光镜下观察可见,缺血4 h后大鼠心肌细胞略肿胀,肌间隙可见少量红细胞漏出;再灌注4 h及6 h后,心肌细胞损伤改变最重;再灌注24 h后,上述改变有所减轻。与正常对照组比较,缺血2 h后,血浆CK-MB的水平即开始明显上升,血浆TnT的水平在缺血4 h后明显上升(P<0.05)。各缺血组血浆H2S的水平及心肌CSE的活性有下降趋势,但无明显统计学差异。与缺血4 h组比较,再灌注0.5 h后血浆CK-MB的水平明显升高,再灌注4 h达高峰;血浆TnT的水平再灌注6 h达高峰;血浆H2S的水平及心肌CSE的活性再灌注2 h后则明显下降,再灌注4 h达最低值;再灌注24 h后,血浆H2S的水平及心肌CSE的活性逐渐回升,血浆CK-MB的水平明显下降(P<0.05)。CK-MB、TnT水平的变化与血浆H2S水平的变化呈明显的负相关。结论 骨骼肌缺血/再灌注可造成心肌损伤,缺血/再灌注4~6 h,心肌损伤最重。内源性血浆H2S/心肌CSE体系的下调可能在骨骼肌再灌注期心肌损伤的病理生理改变中具有重要作用。
Abstract:
AIM To explore the changes of endogenous H2S during myocardial injury caused by ischemia/reperfusion(I/R)of rat skeletal muscle. METHODS We established the model of bilateral hindlimb I/R in rats by using a tourniquet and 62 Wistar rats were divided into 9 groups at random: group normal (C), group 2 h ischemia (I2), group 4 h ischemia (I4) and groups 4 h ischemia with 0.5 h(R0.5), 2 h(R2), 4 h(R4), 6 h(R6), 12 h(R12), 24 h(R24) reperfusion. The pathologic changes in the myocardium were observed. The levels of plasma H2S, CK-MB and TnT in each group were measured and the CSE activity in myocardium was detected. RESULTS Histopathologic results indicated that myocardial injury was relatively mild after skeletal muscle ischemia but it became much more serious following reperfusion. Compared with that in group normal, the level of plasma CK-MB significantly increased in group I2, and the level of plasma TnT markedly increased in group I4(P<0.05). There were no significant changes in H2S and CSE in ischemia groups. Compared with that in group I4, the level of plasma CK-MB markedly increased in group R0.5(P<0.05), reached peak in group R4 and significantly decreased in group R24. The level of plasma TnT markedly increased in group R4, reached peak in group R6 and still remained at high level in group R4. The level of plasma H2S and the level of myocardial CSE decreased obviously in group R2, R4, R6, R12 (P<0.05) and reached the lowest level in group R4. The level of plasma H2S was negatively correlated with the level of plasma CK-MB (r=-0.78, P<0.05) and TnT (r=-0.89, P<0.05). CONCLUSION Skeletal muscle ischemia and reperfusion induce myocardial injury. The injury is the most serious in 4-6 hours after reperfusion. The down-regulation of endogenous H2S/CSE system may play an important role in myocardial injury during skeletal muscle IR.

参考文献/References

[1] Ott MC, Scott JR, Bihari A, et al. Inhalation of carbon monoxide prevents liver injury and inflammation following hind limb ischemia/reperfusion[J] . FASEB J, 2005, 19(1):106-108.[3] Blackstone E, Morrison M, Roth MB. H2S induces a suspended animationlike state in mice[J]. Science, 2005, 308(5721):518.
[4] 张连元,杨林. 生理科学实验教程[M]. 北京: 人民军医出版社, 2001:29-33.
[5] 耿彬,杜军保,唐朝枢. 敏感硫电极法在测定心血管组织细胞及血浆胱硫醚γ裂解酶/硫化氢的应用[J]. 北京大学学报(医学版), 2005, 37(5):545-548.
[6] Zhao W, Zhang J, Lu Y, et al. The vasorelaxant effect of H2S as a novel endogenous gaseous KATP channel opener[J]. EMBO J, 2001, 20(21):6008-6016.
[7] Stipanuk MH, Beck PW. Characterization of the enzymic capacity for cysteine desulphhydration in liver and kidney of the rat[J]. Biochem J, 1982, 206(2):2672-277
[8] Chunyu Z, Junbao D, Dingfang B, et al. The regulatory effect of hydrogen sulfide on hypoxic pulmonary hypertension in rats[J]. Biochem Biophys Res Commun, 2003, 302(4):810-816.
[9] Bian JS, Yong QC, Pan TT, et al. Role of hydrogen sulfide in the cardioprotection caused by ischemic preconditioning in the rat heart and cardiac myocytes. The American Society for Pharmacology and Experimental Therapeutics[J]. J Pharmacol Exp Ther, 2006, 316(2):670-678.
10]Hui Y, Du J, Tang C, et al. Changes in arterial hydrogen sulfide (H2S) content during septic shock and endotoxin shock in rats [J]. J Infect, 2003, 47(2):155-160.

备注/Memo

备注/Memo:
收稿日期:2008-5-14.基金项目:军队“十一五”科技攻关课题项目资助(06G117) 通讯作者:谢晓华,主任医师,教授,主要从事高血压心肌肥厚的防治及创伤应激对心血管系统损伤及保护机理研究Email:n4k@eyou.com 作者简介:陈雯,副主任医师,硕士Email:LHW666@sina.com
更新日期/Last Update: 2009-04-02