Prevention of Myofilament Dysfunction by β-Blocker Therapy in Postinfarct Remodeling
Prevention of Myofilament Dysfunction by β-Blocker Therapy in Postinfarct Remodeling
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DOI：
10.1161/circheartfailure.108.806125
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发表时间：
2009-05-01
影响因子：
9.7
通讯作者：
van der Velden, Jolanda
中科院分区：
文献类型：
--
作者：
Duncker, Dirk J.;Boontje, Nicky M.;van der Velden, Jolanda
背景：在远端非梗死心肌中，个体心肌细胞的肌丝收缩性受到抑制，并导致心肌梗死（MI）后整体左心室泵功能障碍。在这里，我们调查了β-受体阻滞剂治疗是否可以恢复myofilaminescriptive.Methods和结果，在猪心肌梗死引起结扎左回旋支冠状动脉，β-受体阻滞剂治疗（比索洛尔，MI+ β）开始后的第一天MI。在假手术或MI手术后3周进行远程左心室内膜下活检。在单个透化心肌细胞中测量等长力。与假手术组相比，未治疗的MI组的最大力（F-max）较低，而Ca 2+敏感性较高（均P
Background-Myofilament contractility of individual cardiomyocytes is depressed in remote noninfarcted myocardium and contributes to global left ventricular pump dysfunction after myocardial infarction (MI). Here, we investigated whether beta-blocker therapy could restore myofilament contractility.Methods and Results-In pigs with a MI induced by ligation of the left circumflex coronary artery, beta-blocker therapy (bisoprolol, MI+beta) was initiated on the first day after MI. Remote left ventricular subendocardial biopsies were taken 3 weeks after sham or MI surgery. Isometric force was measured in single permeabilized cardiomyocytes. Maximal force (F-max) was lower, whereas Ca2+ sensitivity was higher in untreated MI compared with sham (both P