Physiological Replacement of T3 Improves Left Ventricular Function in an Animal Model of Myocardial Infarction-Induced Congestive Heart Failure
Physiological Replacement of T3 Improves Left Ventricular Function in an Animal Model of Myocardial Infarction-Induced Congestive Heart Failure
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DOI：
10.1161/circheartfailure.108.810747
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发表时间：
2009-05-01
影响因子：
9.7
通讯作者：
Samarel, Allen M.
中科院分区：
文献类型：
--
作者：
Henderson, Kyle K.;Danzi, Sara;Samarel, Allen M.
充血性心力衰竭（CHF）患者血清三碘甲状腺原氨酸（T-3）浓度通常较低。在心肌梗死诱导的CHF和低血清T-3的啮齿动物模型中，我们假设将T-3替换为甲状腺功能正常的水平将改善左心室功能，而不会产生甲状腺毒症的不良体征。方法和结果成年雄性Sprague-Dawley大鼠进行左冠状动脉前降支结扎（心肌梗死）。心肌梗死后一周，CHF动物左心室短轴缩短率显著降低至22 +/- 1%，而假手术对照组为38 +/- 1%（P
Background-Patients with congestive heart failure (CHF) often have low serum triiodothyronine (T-3) concentrations. In a rodent model of myocardial infarction-induced CHF and low serum T-3, we hypothesized that replacing T-3 to euthyroid levels would improve left ventricular function without producing untoward signs of thyrotoxicosis.Methods and Results-Adult male Sprague-Dawley rats were subjected to left anterior descending coronary artery ligation (myocardial infarction). One week post-myocardial infarction, left ventricular fractional shortening was significantly reduced to 22 +/- 1% in CHF animals versus 38 +/- 1% for sham-operated controls (P