Role of myocyte nitric oxide in the contractile dysfunction in heart failure.

心力衰竭与收缩功能障碍和不明原因的心肌细胞水平对β-肾上腺素能刺激的反应性受损有关。心力衰竭增加了心肌中的一氧化氮（NO），这是导致对β-肾上腺素能刺激的收缩反应减弱的原因。在心力衰竭动物模型中，NO与心肌收缩功能异常相关，NO诱导增加可能对充血性心力衰竭心肌收缩功能障碍具有病理生理意义。

Heart failure is associated with the contractile dysfunction and theimpaired responsiveness to beta-adrenergic stimulation at the myocyte level of unknown causes. Heart failure increased nitric oxide (NO) in the myocardium, which was responsible for the diminished contractile responses to beta-adrenergic stimulation. The association of NO and contractile abnormalities was recognized in the animal model of failing heart and increased NO induction might have pathophysiological significance for the contractile defects in congestive heart failure.