硫化氢对截肢创伤后心肌线粒体功能的保护作用
《心脏杂志》[ISSN:1009-7236/CN:61-1268/R]
- 期数:
- 2009年第3期
- 页码:
- 340-342,350
- 栏目:
- 基础研究
- 出版日期:
- 2009-05-15
文章信息/Info
- Title:
- Protective effect of hydrogen sulfide on myocardial mitochondrion function after amputated extremity trauma
- Author(s):
- REN Qing-ai; XIE Xiao-hua; ZHANG Hai-feng; ZHANG Ying
- First Department of Comprehensive Surgery, South Building, PLA General Hospital, Beijing 100853, China
- Keywords:
- mitochondrion; hydrogen sulfide; trauma; energy metabolism
- 分类号:
- R329.24
- DOI:
- -
- 文献标识码:
- A
- 摘要:
- 目的 探讨外源性H2S对截肢创伤应激后心肌线粒体功能的影响，以及截肢创伤应激后，心肌线粒体损伤与H2S对心肌线粒体功能的保护作用。方法 建立截肢创伤应激模型。雄性SD大鼠48只（平均体质量260～300 g），分为正常对照组、创伤组（截肢后6 h）、NaHS组（截肢后立即腹腔注射NaHS 28 μmol/kg，6 h后处死）和炔丙基甘氨酸（PPG）组（截肢后立即给予腹腔注射PPG 50 mg/kg，6 h后处死），每组8只。提取心肌线粒体，用strathkelvin氧电极法测定线粒体的呼吸功能。用罗丹明123(Rh123)荧光测定线粒体的膜电位，用微量ATP酶试剂盒检测线粒体总ATP的变化。结果 与正常对照组比，创伤后心肌线粒体的呼吸功能受损［呼吸控制率(RCR)及磷氧比(P/O)降低，P<0.05］，膜电位下降（P<0.05），总ATP酶的含量降低（P<0.05）。与创伤组比，NaHS组心肌线粒体的呼吸功能改善（RCR、P/O升高，P<0.05），膜电位升高（P<0.05），总ATP酶的含量增加（P<0.05）。PPG组心肌线粒体的呼吸功能进一步受损（RCR、P/O降低，P<0.05），总ATP酶的含量减少（P<0.05）。结论 截肢创伤应激可使心肌线粒体的呼吸功能受损，膜电位下降，能量代谢障碍，硫化氢对截肢创伤后心肌线粒体的损伤具有保护作用。
- Abstract:
- AIM To investigate the influence of hydrogen sulfide on myocardial mitochondrion function after amputated extremity trauma and to probe the injury of mitochondrion and the protection of H2S on myocardial mitochondrion function of after amputated extremity trauma. METHODS Weight-matched adult male SD rats were randomly divided into 4 groups: the control group (n=8), the trauma group (n=8): 6 h after amputated trauma, NaHS group (n=8): NaHS solution intraperitoneal injection (28 μmol/kg), and PPG group (n=8): PPG solution (50 mg/kg). Strathkelvin Model 782 Oxgen meter was used to determine the respiratory function of mitochondrion and membrane potential was detected by rhodamine. RESULTS Compared with that in the control group, the respiratory function of mitochondrion was damaged after trauma. The membrane potential and the content of ATP in mitochondrion were depressed. Compared with that in the trauma group, the respiratory function was improved but the membrane potential and the content of ATP in mitochondrion were depressed in NaHS group. CONCLUSION The respiratory function of myocardial mitochondrion is damaged and energy metabolism is disturbed after amputated trauma. Hydrogen sulfide provides some protection for myocardial mitochondrion after amputated trauma.
参考文献/References
[1］ Yang S, Hu S, Hsieh YC, et al. Mechanism of IL-6-mediated cardiac dysfunction following trauma-hemorrhage［J］. J Mol Cell Cardiol, 2006, 40(4):570-579.
［2］ Cossarizza A. Tests for mitochondrial function and DNA: potentials and pitfalls［J］. Curr Opin Infect Dis, 2003, 16(1):5-10.
［3］ 钱令嘉,弓景波,程素琦. 热应激心肌细胞损伤的线粒体机制探讨［J］. 中国应用生理学杂志, 2000, 16(2):133-136.
［4］ Johansen D, Ytrehus K, Baxter GF. Exogenous hydrogen sulfide (H2S) protects against regional myocardial ischemia-reperfusion injury-Evidence for a role of KATP channels［J］. Basic Res Cardiol, 2006, 101(1):53-60.
［5］ Hengartner MO. The biochemistry of apoptosis［J］. Nature, 2000, 407(6805):770-776.
［6］ O’Rourke B. Myocardial KATP channels in preconditioning［J］. Circ Res, 2000, 87(10):845-855.
［7］ Blackstone E, Morrison M, Roth MB. H2S induces a suspended animation-like state in mice［J］. Science, 2005, 308(5721):518.
［8］ Geng B, Chang L, Pan C, et al. Endogenous hydrogen sulfide regulation of myocardial injury induced by isoproterenol［J］. Biochem Biophys Res Commun, 2004, 318(3):756-763.
［9］ Akao M, Ohler A, O’Rourke B. Mitochondrial ATP-sensitive potassium channels inhibit apoptosis by oxidative stress in cardiac cells［J］. Circ Res, 2001, 88(12):1267-1275.
［10］Liu Y, Sato T, Seharaseyon J, et al. Mitochondrial ATP-dependent potassium channels: viable candidateeffectors of ischemic preconditioning［J］. Ann N Y Acad Sci, 1999, 874:27-37.
备注/Memo
- 备注/Memo:
- 收稿日期：2008-10-12.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，主要从事围手术期心血管保护研究Email:n4k@eyou.com 作者简介：任青爱，主治医师，硕士Email:ren19762@sina.com
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