期刊文献+

Ca^(2+)在严重烧伤早期心肌线粒体呼吸功能损害中的作用及其机制研究 被引量:4

Role of Ca^(2+) in the damage of myocardial mitochondrial respiratory function in the early stage after severe burns
暂未订购
导出
摘要 目的 探讨Ca2 + 在严重烧伤早期心肌线粒体呼吸功能损害中的作用及其机制。方法 复制 30 %TBSAⅢ度烧伤大鼠模型 ,取正常及伤后 1、3、6、12、2 4h大鼠心肌分离线粒体 ,测其Ca2 + 浓度 ( [Ca2 + ]m)、线粒体PLA2 (mtPLA2 )、一氧化氮合酶 (mtNOS)、F0 F1 ATPase和细胞色素c氧化酶活性 ,同时观察心肌线粒体呼吸功能变化。结果 ①伤后 1h [Ca2 + ]m与线粒体呼吸控制率(RCR)均明显升高 ,且RCR与 [Ca2 + ]m呈显著正相关 ;伤后 3、6、12、2 4h心肌 [Ca2 + ]m、mtPLA2 及mtNOS活性均显著高于正常组 ,但线粒体呼吸功能反而下降 ,RCR与 [Ca2 + ]m呈明显负相关 ,mtNOS、mtPLA2 活性与 [Ca2 + ]m呈明显正相关。②伤后 1h线粒体F0 F1 ATPase合成活性明显升高 ,但 3、6、12、2 4h其合成活性与细胞色素c氧化酶活性均显著低于正常组 ;F0 F1 ATPase水解活性除伤后 3h显著升高外 ,其余各时相点均明显低于正常对照组。结论  [Ca2 + ]m改变是烧伤后心肌线粒体呼吸功能变化的重要原因 ,烧伤初始 [Ca2 + ]m适度升高 ,促进线粒体呼吸功能加强 ;烧伤后续阶段Ca2 + 严重超载激活mtPLA2 。 Objective To explore the role of Ca 2+ in the damage of myocardial mitochondrial respiratory function in the early stage after severe burns. Methods An experimental model of 30%TBSA full thickness skin scalding was established in rats. Myocardial mitochondira were isolated from control rats and burned rats at the 1, 3, 6, 12 and 24 h postburn. Changes of mitochondrial respiratory function were observed, Contents of mitochondrial calcium([Ca 2+ ]m),activities of mtPLA 2 , mtNOS, F 0 F 1 ATPase, and cytochrome coxidase were determined. Results ① At 1 h postburn, [Ca 2+ ]m and mitochondrial respiratory control rate (RCR) were both elevated significantly, and RCR was postively correlated with [Ca 2+ ]m. At 3, 6, 12, and 24 h postburn, [Ca 2+ ]m and the activities of mtNOS and mtPLA 2 were significantly higher than those of the controls, but the mitochondrial respiratory function of burned rats decreased, and RCR was negatively correlated with [Ca 2+ ]m, while mtNOS and mtPLA 2 activities were both positively correlated with [Ca 2+ ]m. ②The F 0 F 1 ATPase synthetic activity increased at the 1st hour postburn, but it and the cytochrome coxidase activity both decreased at 3, 6, 12 and 24 h postburn. Except for elevation at 3 h postburn, the F 0 F 1 ATPase hydrolytic activity decreased at all other time points. Conclusions The changes of [Ca 2+ ]m were involved in the damage or regulation of mitochondrial respiratory function after severe burns. Appropriate increase of [Ca 2+ ]m reinforced the mitochondrial respiration fumctionin the beginning statge after severe burns, but activation of mtPLA 2 and mtNOS by severe overloading of Ca 2+ might play an important role in the damages of myocardial mitochondria respiratory function in the following stage after severe burns.
出处 《第三军医大学学报》 CAS CSCD 北大核心 2002年第2期135-137,共3页 Journal of Third Military Medical University
基金 国家重点基础研究发展规划项目 ("973"项目 ) (G19990 54 2 0 2 )
关键词 烧伤 线粒体 心肌 burns mitochondria Ca 2+ myocardium
  • 相关文献

参考文献10

  • 1Huang Y S, Yang Z C, Yan B G. Pathogenesis of early cardiac myocyte damage after severe burns[J]. J Trauma, 1999,46(3):428-432.
  • 2梁晚益,杨宗城,黄跃生.大鼠严重烧伤早期心肌线粒体Ca^(2+)转运变化及其机制研究[J].第三军医大学学报,2001,23(1):45-47. 被引量:6
  • 3梁晚益,杨宗城,黄跃生.mtPLA_2在严重烧伤早期心肌线粒体损害中的作用[J].第三军医大学学报,2000,22(3):210-212. 被引量:7
  • 4Zaidan E, Sims N R. Reduced activity of the pyruvate dehydrogenase complex but not cytochrome coxidase is associated with neuronal loss in the striatum following short-term forebrain ischemia[J]. Brain Res,1997,772(1-2):23-28.
  • 5Yamada E W, Huzel N J. Calcium-binding ATPase inhibitor protein of bovine heart mitochondria. Role in ATP synthesis and effect of Ca2+[J]. Biochemistry,1989,28(25):9 714-9 718 .
  • 6Horton J W, Garcia N M, White D J,et al. Postburn cardiac contractile function and biochemical markers of postburn cardiac injury[J]. J Am Coll Surg,1995,181(4):289-298.
  • 7Robb Gaspers L D, Rutter G A, Burnett P,et al. Coupling between cytosolic and mitochondrial calcium oscillations: role in the regulation of hepatic metabolism[J]. Biochim Biophys Acta,1998,1 366(1-2):17-32.
  • 8Levrat C, Louisot P. Increase of mitochondrial PLA2-released fatty acidsis an early event in tumor necrosis factor alpha-treated WEHI-164 cells[J]. Biochem Biophys Res Commun,1996,221(3):531-538.
  • 9梁晚益,杨宗城,黄跃生.NO在外源性高浓度Ca^(2+)损伤心肌线粒体中的作用[J].中国病理生理杂志,2000,16(12):1292-1294. 被引量:9
  • 10Brookes P S, Bolanos J P, Heales S J. The assumption that nitric oxide inhibits mitochondrial ATP synthesisis correct[J]. FEBS Lett,1999,446(2-3):261-263.

二级参考文献7

共引文献17

同被引文献28

  • 1张卫国,张志善.丹皮酚对大鼠心肌缺血再灌注损伤的线粒体膜脂的保护作用[J].中草药,1994,25(4):193-194. 被引量:7
  • 2杨天德,刘桥义,王舟琪,胡成舫.纳络酮对缺血再灌注心肌儿茶酚胺释放的影响[J].中华麻醉学杂志,1994,14(5):331-333. 被引量:10
  • 3杨天德,刘桥义,王舟琪.纳络酮对缺血再灌注心肌脂质过氧化物和钙含量的影响[J].现代应用药学,1996,13(3):3-5. 被引量:5
  • 4苟俊 李才安.大鼠线粒体脂肪酸的气相色谱分析[J].第三军医大学学报,1992,7:149-151.
  • 5Kashimoto S,Hinohara S,Kumazawa T. Effects of naloxone on cardiac energy metabolism in hypovolemic shock in rats[J]. Resuscitation, 1989,17(1) : 33.
  • 6Kashimoto S, Hinohara S, Miyaji T,et al. Effects of naloxone on cardiac energy metabolism in acute hemorrhage in rats[J]. Resuscitation, 1986,14 (3) : 157.
  • 7Yang CS, Tsai PJ ,Chen WY, et al. Increased formation of interstitial hydroxyl radical following myocardial ischemia: possible relationship to endogenous opioid peptides[J]. Redox Rep, 1997, 3(5-6) :295.
  • 8Wang Y,Ashraf M.Role of protein kinase - C in mitochondria KATP channel mediated protection against Ca2 + overload injury in rat myocardium.Circ Res,1999,84:1156 - 1165.
  • 9Halestrap AP.The regulation of the matrix volume of mammalian mitochondria in vivo and in vitro and its role in the control of mitochondria metabolism .Biochim Biophys Acta,1989,973:355 - 382.
  • 10Holmuhamedov EL,Wang L,Terzic A.ATP sensitive K^+ channel openers prevent Ca^2+ overload in rat cardiac mitochondria .J Physiol,1999,519:347 - 360.

引证文献4

二级引证文献12

相关作者

内容加载中请稍等...

相关机构

内容加载中请稍等...

相关主题

内容加载中请稍等...

浏览历史

内容加载中请稍等...
;
使用帮助 返回顶部