Role of myocardial neuronal nitric oxide synthase-derived nitric oxide in β-adrenergic hyporesponsiveness after myocardial infarction-induced heart failure in rat
Role of myocardial neuronal nitric oxide synthase-derived nitric oxide in β-adrenergic hyporesponsiveness after myocardial infarction-induced heart failure in rat
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DOI：
10.1161/01.cir.0000145160.04084.ac
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发表时间：
2004-10-19
期刊：
影响因子：
37.8
通讯作者：
Heymes, C
中科院分区：
文献类型：
--
作者：
Bendall, JK;Damy, T;Heymes, C
背景-一个新兴的概念是一氧化氮合酶（NOS 1）的神经亚型可以调节心肌收缩力。方法和结果：采用心肌梗死诱导的心力衰竭模型，我们证明心力衰竭大鼠心脏NOS 1表达和活性增加（P < 0.05和P <0.05），心肌NOS 1表达和活性增加（P < 0.05），心肌NOS 1活性增加（P < 0.05），心肌NOS 1活性增加（P < 0.05），心肌NOS 1活性增加（P <0.05）。
Background - An emerging concept is that a neuronal isoform of nitric oxide synthase (NOS1) may regulate myocardial contractility. However, a role for NOS1-derived nitric oxide (NO) in heart failure (HF) has not been defined.Methods and Results - Using a model of myocardial infarction-induced HF, we demonstrated that cardiac NOS1 expression and activity increased in HF rats (P < 0.05 and P