McMahon W S, Mukherjee R, Gillette P C, Crawford F A, Spinale F G
Division of Pediatric Cardiology, Medical University of South Carolina, Charleston 29425, USA.
Cardiovasc Res. 1996 Feb;31(2):314-23.
Comparison of the effects of supraventricular tachycardia-induced dilated cardiomyopathy on left and right ventricular isolated myocyte geometry and function.
Chronic ventricular tachycardia and supraventricular tachycardia cause left ventricular dilation and dysfunction in humans. However, it is unknown whether supraventricular tachycardia-induced dilated cardiomyopathy is a homogenous process for both the left and right ventricles.
Dilated cardiomyopathy was induced by rapid atrial pacing (240 beats/min, 3 weeks) in 5 pigs. Five age- and weight-matched pigs served as controls. Ventricular mass was measured, myocyte dimensions were obtained, and isolated right and left ventricular myocyte contractile performance was evaluated at baseline and after beta-adrenergic receptor stimulation.
With the development of dilated cardiomyopathy, there was no change in left ventricular mass. In contrast, right ventricular mass was increased, as was right ventricular myocyte cross-sectional area. In the control group, baseline right ventricular myocyte contractile function was increased compared to left ventricular myocytes. beta-adrenergic receptor stimulation increased myocyte contractile function in both left and right ventricular myocytes. With supraventricular tachycardia-induced cardiomyopathy, both left and right ventricular myocyte contractile function and beta-adrenergic responsiveness were reduced.
This study demonstrated differences in left and right ventricular myocyte growth with supraventricular tachycardia-induced dilated cardiomyopathy and this differential growth response was associated with changes in contractile performance. Thus, in this model of cardiomyopathic disease, left and right ventricular growth and changes in contractile performance are not a homogenous process.
比较室上性心动过速诱发的扩张型心肌病对左、右心室分离心肌细胞几何形状和功能的影响。
慢性室性心动过速和室上性心动过速可导致人类左心室扩张和功能障碍。然而,尚不清楚室上性心动过速诱发的扩张型心肌病对左、右心室而言是否为同质过程。
对5头猪进行快速心房起搏(240次/分钟,3周)以诱发扩张型心肌病。5头年龄和体重匹配的猪作为对照。测量心室质量,获取心肌细胞尺寸,并在基线时以及β-肾上腺素能受体刺激后评估分离的右心室和左心室心肌细胞的收缩性能。
随着扩张型心肌病的发展,左心室质量无变化。相比之下,右心室质量增加,右心室心肌细胞横截面积也增加。在对照组中,基线时右心室心肌细胞的收缩功能比左心室心肌细胞增强。β-肾上腺素能受体刺激使左、右心室心肌细胞的收缩功能均增强。在室上性心动过速诱发的心肌病中,左、右心室心肌细胞的收缩功能和β-肾上腺素能反应性均降低。
本研究证明了室上性心动过速诱发的扩张型心肌病中左、右心室心肌细胞生长存在差异,这种差异生长反应与收缩性能的变化有关。因此,在这种心肌病模型中,左、右心室的生长以及收缩性能的变化并非同质过程。