• 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>Life sciences >Inhibition of ischemia/reperfusion-induced damage by dexamethasone in isolated working rat hearts: the role of cytochrome c release
【24h】

Inhibition of ischemia/reperfusion-induced damage by dexamethasone in isolated working rat hearts: the role of cytochrome c release

机译：地塞米松对离体大鼠的心脏缺血/再灌注损伤的抑制作用：细胞色素c释放的作用

获取原文
获取原文并翻译 | 示例
           
页面导航
  • 摘要
  • 著录项
  • 相似文献
  • 相关主题

摘要

We investigated the contribution of dexamethasone treatment on the recovery of postischemic cardiac function and the development of reperfusion-induced arrhythmias in ischemic/reperfused isolated rat hearts. Rats were treated with 2 mg/kg of intraperitoneal injection of dexamethasone, and 24 hours later, hearts were isolated according to the 'working' mode, perfused, and subjected to 30 min global ischemia followed by 120 min reperfusion. Cardiac function including heart rate, coronary flow, aortic flow, and left ventricular developed pressure were recorded. After 60 min and 120 min reperfusion, 2 mg/kg of dexamethasone significantly improved the postischemic recovery of aortic flow and left ventricular developed pressure from their control values, of 10.7 +/- 0.3 ml/min and 10.5 +/- 0.3 kPa to 22.2 +/- 0.3 ml/min (p<0.05) and 14.3 +/- 0.5 kPa (p<0.05), 19.3 +/- 0.3 ml/min (p<0.05) and 12.3 +/- 0.5 kPa (p<0.05), respectively. Heart rate and coronary flow did not show a significant change in postischemic recovery after 60 or 120 min reperfusion. In rats treated with 0.5 mg/kg of actinomycin D injected i.v., one hour before the dexamethasone injection, suppressed the dexamethasone-induced cardiac protection. Electrocardiograms were monitored to determine the incidence of reperfusion-induced ventricular fibrillation. Dexamethasone pretreatment significantly reduces the occurrence of ventricular fibrillation. Cytochrome c release was also observed in the cytoplasm. The results suggest that the inhibition of cytochrome c release is involved in the dexamethasone-induced cardiac protection. (C) 2004 Elsevier Inc. All rights reserved.
机译：我们调查了地塞米松治疗对缺血/再灌注离体大鼠心脏缺血后心脏功能恢复和再灌注诱发心律不齐的发展的贡献。用2 mg / kg腹腔注射地塞米松治疗大鼠，然后24小时后，按照“工作”模式分离心脏，进行灌注，并进行30分钟的整体缺血，然后再进行120分钟的再灌注。记录心功能，包括心率，冠状动脉血流，主动脉血流和左心室发育压力。再灌注60分钟和120分钟后，地塞米松2 mg / kg的缺血性恢复能力从其控制值10.7 +/- 0.3 ml / min和10.5 +/- 0.3 kPa的正常值显着改善了主动脉血流和左心室形成压力至22.2 +/- 0.3 ml / min（p <0.05）和14.3 +/- 0.5 kPa（p <0.05），19.3 +/- 0.3 ml / min（p <0.05）和12.3 +/- 0.5 kPa（p <0.05） ， 分别。再灌注60或120分钟后，心率和冠状动脉血流没有显示缺血后恢复的显着变化。在地塞米松注射前一小时，用0.5 mg / kg放线菌素D静脉注射治疗的大鼠抑制了地塞米松诱导的心脏保护作用。监测心电图以确定再灌注引起的心室纤颤的发生率。地塞米松预处理可显着减少心室纤颤的发生。在细胞质中也观察到细胞色素c的释放。结果表明，细胞色素c释放的抑制与地塞米松诱导的心脏保护有关。 （C）2004 Elsevier Inc.保留所有权利。

著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
获取原文

客服邮箱：kefu@zhangqiaokeyan.com

京公网安备：11010802029741号 ICP备案号：京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有

  • 客服微信

  • 服务号