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首页> 外文期刊>Journal of Molecular and Cellular Cardiology >In vivo and in vitro cardiac responses to beta-adrenergic stimulation in volume-overload heart failure.
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In vivo and in vitro cardiac responses to beta-adrenergic stimulation in volume-overload heart failure.

机译：体内和体外心脏对β-肾上腺素能刺激的反应在容量超负荷心力衰竭中。

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Hearts in volume overload (VO) undergo progressive ventricular hypertrophy resulting in chronic heart failure that is unresponsive to β-adrenergic agonists. This study compared left ventricular (LV) and isolated cardiomyocyte contractility and β-adrenergic responsiveness in rats with end-stage VO heart failure (HF). Adult male Sprague-Dawley rats were studied 21 weeks after aortocaval fistula (ACF) or sham surgery. Echocardiography revealed decreased fractional shortening accompanied by increased LV chamber diameter and decreased eccentric dilatation index at end-stage ACF compared to sham. Hemodynamic measurements showed a decrease in the slope of end-systolic pressure-volume relationship, indicating systolic dysfunction. Isolated LV myocytes from ACF exhibited decreased peak sarcomere shortening and kinetics. Both Ca2+ transient amplitude and kinetics were increased in ACF myocytes, with no change under the integrated Ca2+ curves relating to contraction and relaxation phases. Increases in ryanodine receptor and phospholamban phosphorylation, along with a decrease in SERCA2 levels, were observed in ACF. These changes were associated with decreased expression of β-myosin heavy chain, cardiac troponin I and cardiac myosin binding protein-C. In vivo inotropic responses to β-adrenergic stimulation were attenuated in ACF. Interestingly, ACF myocytes exhibited a similar peak shortening to those of sham in response to a β-adrenergic agonist. The protein expression of the gap junction protein connexin-43 was decreased, although its phosphorylation at Ser-368 increased. These changes were associated with alterations in Src and ZO-1. In summary, these data suggest that the disconnect in β-adrenergic responsiveness between in vivo and in vitro conditions may be associated with altered myofilament Ca2+ sensitivity and connexin-43 degradation.
机译：容量超负荷（VO）的心脏进行性心室肥大，导致慢性心力衰竭，对β肾上腺素激动剂无反应。这项研究比较了晚期VO心力衰竭（HF）大鼠的左心室（LV）和孤立的心肌收缩力以及β-肾上腺素能反应性。成年雄性Sprague-Dawley大鼠在进行主动脉腔瘘（ACF）或假手术后21周进行了研究。超声心动图显示，与假手术相比，末期ACF的缩短分数减少，伴随着左室直径增加和偏心扩张指数降低。血液动力学测量结果显示收缩末期压力-容积关系的斜率降低，表明收缩期功能障碍。从ACF分离的LV心肌细胞表现出减少的峰值肌节缩短和动力学。在ACF心肌细胞中，Ca2 +的瞬时振幅和动力学均增加，在与收缩和松弛期有关的完整Ca2 +曲线下没有变化。在ACF中观察到了莱丹碱受体和磷酸lamban磷酸化的增加，以及SERCA2水平的降低。这些变化与β-肌球蛋白重链，心肌肌钙蛋白I和心肌肌球蛋白结合蛋白-C的表达降低有关。在ACF中，体内对β-肾上腺素能刺激的正性肌力反应减弱。有趣的是，响应于β-肾上腺素能激动剂，ACF心肌细胞显示出与假手术相似的峰缩短。间隙连接蛋白连接蛋白43的蛋白表达降低，尽管其在Ser-368的磷酸化增加。这些变化与Src和ZO-1的改变有关。总之，这些数据表明体内和体外条件之间β-肾上腺素反应性的断开可能与肌丝Ca 2+敏感性改变和连接蛋白43降解有关。

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