• 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>Life sciences >DITPA restores the repolarizing potassium currents I-tof and I-ss in cardiac ventricular myocytes of diabetic rats
【24h】

DITPA restores the repolarizing potassium currents I-tof and I-ss in cardiac ventricular myocytes of diabetic rats

机译：DITPA可恢复糖尿病大鼠心室肌细胞的复极钾电流I-tof和I-ss

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

Diabetes Mellitus (DM) can produce an increase in the cardiac action potential duration and QT interval that can be associated with sudden death. These cardiac effects are due to a region-specific decrease in repolarizing outward K+ currents. Some authors have suggested that the proarrhythmic effects of diabetes can be due to diabetes-induced hypothyroidism. Thus, we have examined the effect of the thyroid hormone analog diiodothyropropionic acid (DITPA) on calcium-independent outward potassium currents in ventricular myocytes from diabetic rats. Sustained (I-ss) and fast transient outward (I-tof) K+ currents were recorded using the whole-cell configuration of the patch-clamp technique. Myocytes were enzymatically isolated from the free wall of the right ventricle, and the epicardial and endocardial layers of the left ventricle of healthy, diabetic and DITPA-treated diabetic rats. Circulating thyroid hormones were measured by electrochemiluminescence. DITPA-treatment of diabetic rats restored I-tof and I-ss current densities in cardiac myocytes from the three regions studied, but did not alter current densities in myocytes of control rats. T-3 and T-4 levels were reduced by diabetes, and DITPA-treatment increased circulating T-3 levels. T-3-treatment of diabetic rats also restored current densities to control values. However, direct incubation of diabetic myocytes with DITPA did not restore current densities. In summary, DITPA-treatment of diabetic rats restored the potassium current (I-tof and I-ss) densities in myocytes from all ventricular regions. (c) 2006 Elsevier Inc. All rights reserved.
机译：糖尿病（DM）会使心脏动作电位持续时间和QT间隔增加，这可能与猝死有关。这些心脏效应是由于向外极化的K +电流重新极化时特定区域的减少所致。一些作者建议，糖尿病的心律失常可能是由于糖尿病引起的甲状腺功能减退。因此，我们已经检查了甲状腺激素类似物二碘甲状腺丙酸（DITPA）对糖尿病大鼠心室肌细胞中钙非依赖性向外钾电流的影响。使用膜片钳技术的全电池配置记录持续（I-ss）和快速瞬态向外（I-tof）K +电流。从健康，糖尿病和DITPA治疗的糖尿病大鼠的右心室自由壁以及左心室的心外膜和心内膜层中酶分离心肌细胞。通过电化学发光测量循环甲状腺激素。 DITPA治疗的糖尿病大鼠从研究的三个区域恢复了心肌细胞的I-tof和I-ss电流密度，但没有改变对照大鼠的心肌细胞的电流密度。糖尿病降低了T-3和T-4的水平，而DITPA治疗增加了循环T-3的水平。糖尿病大鼠的T-3-治疗也使电流密度恢复到控制值。然而，将糖尿病心肌细胞与DITPA直接温育不能恢复电流密度。总之，DITPA治疗的糖尿病大鼠恢复了所有心室区域心肌细胞的钾电流密度（I-tof和I-sss）。 （c）2006 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