...
  • 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>Anesthesiology >Differential role of calcium/calmodulin-dependent protein kinase II in desflurane-induced preconditioning and cardioprotection by metoprolol: metoprolol blocks desflurane-induced preconditioning.
【24h】

Differential role of calcium/calmodulin-dependent protein kinase II in desflurane-induced preconditioning and cardioprotection by metoprolol: metoprolol blocks desflurane-induced preconditioning.

机译：钙/钙调蛋白依赖性蛋白激酶II在地氟醚诱导的预处理和美托洛尔的心脏保护中的不同作用：美托洛尔阻断地氟醚诱导的预处理。

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

BACKGROUND: Anesthetic preconditioning is mediated by beta- adrenergic signaling. This study tested the hypotheses that desflurane-induced preconditioning is dose-dependently blocked by metoprolol and mediated by calcium/calmodulin-dependent protein kinase II (CaMK II). METHODS: Pentobarbital-anesthetized New Zealand White rabbits were instrumented for measurement of systemic hemodynamics and subjected to 30 min of coronary artery occlusion followed by 3 h of reperfusion. Rabbits were assigned to receive vehicle (control), 0.2, 1.0, 1.75, or 2.5 mg/kg metoprolol for 30 min, or the CaMK II inhibitor KN-93 in the absence or presence of 1.0 minimum alveolar concentration desflurane. Protein expression of CaMK II, phospholamban, and phospho-phospholamban was measured by Western blotting. Myocardial infarct size and area at risk were measured with triphenyltetrazolium staining and patent blue, respectively. RESULTS: Baseline hemodynamics were not different among groups. Infarct size was 60 +/- 3% in controland significantly (* P < 0.05) decreased to 33 +/- 2%* by desflurane. The CaMK II inhibitor KN-93 did not affect infarct size (55 +/- 4%) but blocked desflurane-induced preconditioning (57 +/- 3%). Metoprolol at 0.2 and 1.0 mg/kg had no effect on infarct size (55 +/- 3% and 53 +/-3%), whereas metoprolol at 1.75 and 2.5 mg/kg reduced infarct size to 48 +/- 4%* and 39 +/- 5%*, respectively. Desflurane-induced preconditioning was attenuated by metoprolol at 0.2 mg/kg, leading to an infarct size of 46 +/- 5%*, and was completely abolished by metoprolol at 1.0, 1.75, and 2.5 mg/kg, resulting in infarct sizes of 51 +/- 3%, 52 +/- 3%, and 55 +/- 3%, respectively. CONCLUSIONS: Desflurane-induced preconditioning is dose-dependently blocked by metoprolol and mediated by CaMK II.
机译：背景：麻醉药的预处理是由β-肾上腺素能信号传导介导的。这项研究检验了以下假说：地氟醚诱导的预处理被美托洛尔剂量依赖性地阻断，并被钙/钙调蛋白依赖性蛋白激酶II（CaMK II）介导。方法：将戊巴比妥麻醉的新西兰白兔用于全身血流动力学的测量，并进行30分钟的冠状动脉闭塞，然后再灌注3 h。在不存在或存在1.0最低肺泡浓度地氟醚的情况下，将兔子分配为接受媒介物（对照），0.2、1.0、1.75或2.5 mg / kg美托洛尔30分钟，或接受CaMK II抑制剂KN-93。 CaMK II，phospholamban和phospho-phospholamban的蛋白质表达通过蛋白质印迹法测量。分别用三苯基四唑鎓染色和漆蓝测量心肌梗塞的大小和危险区域。结果：各组之间的基线血流动力学无差异。对照的梗塞面积为60 +/- 3％，地氟醚显着（* P <0.05）降低至33 +/- 2％*。 CaMK II抑制剂KN-93不会影响梗塞面积（55 +/- 4％），但会阻止地氟醚诱导的预处理（57 +/- 3％）。 0.2和1.0 mg / kg的美托洛尔对梗塞面积没有影响（55 +/- 3％和53 +/- 3％），而1.75和2.5 mg / kg的美托洛尔将梗塞面积减少到48 +/- 4％*和39 +/- 5％*。地氟醚诱导的预处理被0.2 mg / kg的美托洛尔减弱，导致梗死面积为46 +/- 5％*，而被美托洛尔的1.0、1.75和2.5 mg / kg完全消除，导致梗死面积为51 +/- 3％，52 +/- 3％和55 +/- 3％。结论：地氟醚诱导的预处理被美托洛尔剂量依赖性地阻断并且由CaMK II介导。

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