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首页> 外文期刊>American Journal of Physiology >Functional alterations after cardiac sodium-calcium exchanger overexpression in heart failure.
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Functional alterations after cardiac sodium-calcium exchanger overexpression in heart failure.

机译：心力衰竭中心脏钠钙交换剂过表达后的功能改变。

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The sodium-calcium exchanger (NCX) is discussed as one of the key proteins involved in heart failure. However, the causal role and the extent to which NCX contributes to contractile dysfunction during heart failure are poorly understood. NCX overexpression was induced by infection with an adenovirus coding for NCX, which coexpressed green fluorescence protein (GFP) (AdNCX) by ex vivo gene transfer to nonfailing and failing rabbit cardiomyocytes. Myocardial gene transfer in rabbits in vivo was achieved by adenoviral delivery via aortic cross-clamping. Peak cell shortening of cardiomyocytes was determined photo-optically. Hemodynamic parameters in vivo were determined by echocardiography (fractional shortening) and tip catheter [maximal first derivative of left ventricular (LV) pressure (dP/dt(max)); maximal negative derivative of LV pressure (-dP/dt(max))]. Peak cell shortening was depressed after NCX gene delivery in isolated nonfailing and in failing cardiomyocytes. In nonfailing rabbits in vivo, basal systolic contractility (fractional shortening and dP/dt(max)) and maximum rate of LV relaxation (-dP/dt(max)) in vivo were largely unaffected after NCX overexpression. However, during heart failure, long-term NCX overexpression over 2 wk significantly improved fractional shortening and dP/dt(max) compared with AdGFP-infected rabbits, both without inotropic stimulation and after beta-adrenergic stimulation with isoproterenol. -dP/dt(max) was also improved after NCX overexpression in the failing rabbits group. These results indicate that short-term effects of NCX overexpression impair contractility of isolated failing and nonfailing rabbit cardiomyocytes. NCX overexpression over 2 wk in vivo does not seem to affect myocardial contractility in nonfailing rabbits. Interestingly, in vivo overexpression of NCX decreased the progression of systolic and diastolic contractile dysfunction and improved beta-adrenoceptor-mediated contractile reserve in heart failure in rabbits in vivo.
机译：钠钙交换剂（NCX）被讨论为涉及心力衰竭的关键蛋白质之一。但是，人们对NCX在心力衰竭期间导致收缩功能障碍的起因作用和程度了解甚少。 NCX的过表达是由编码NCX的腺病毒感染引起的，该腺病毒通过离体基因转移到未失败和衰竭的兔心肌细胞中共表达绿色荧光蛋白（GFP）（AdNCX）。兔体内活体心肌基因的转移是通过腺病毒通过主动脉交叉钳夹实现的。用光学方法确定心肌细胞的峰值细胞缩短。通过超声心动图（分数缩短）和尖端导管[左心室（LV）压力的最大一阶导数（dP / dt（max））确定体内血液动力学参数。 LV压力的最大负导数（-dP / dt（max））]。 NCX基因传递后，在孤立的未失败和衰竭的心肌细胞中，峰值细​​胞缩短被抑制。在体内未失败的兔子中，NCX过表达后，基本收缩收缩力（分数缩短和dP / dt（max））和体内左室最大舒张率（-dP / dt（max））基本不受影响。但是，在心力衰竭期间，与无Adotropic刺激和异丙肾上腺素β-肾上腺素刺激后相比，长期超过2周的NCX过度表达显着改善了分数缩短和dP / dt（max）。在衰竭兔子组中NCX过表达后，-dP / dt（max）也得到改善。这些结果表明，NCX过表达的短期影响削弱了孤立的衰竭和非衰竭兔心肌细胞的收缩能力。体内超过2周的NCX过表达似乎不会影响未衰竭兔子的心肌收缩力。有趣的是，体内NCX的过表达降低了兔子心衰时收缩压和舒张收缩功能障碍的进展，并改善了β-肾上腺素受体介导的收缩储备。

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