Harding S E, Brown L A, del Monte F, Davies C H, O'Gara P, Vescovo G, Wynne D G, Poole-Wilson P A
National Heart & Lung Institute, Dept. Cardiac Medicine, London, UK.
Basic Res Cardiol. 1996;91 Suppl 2:53-6. doi: 10.1007/BF00795363.
Myocytes from failing human ventricle contract and relax more slowly than those from non-failing. This has been suggested to result from the lowering of basal cyclic AMP level in failing myocardium, and the consequent withdrawal of a tonic lusitropic effect. We present data to support this hypothesis by demonstrating that the acceleration of contraction and relaxation by beta-adrenoceptor stimulation is greater in myocytes from failing than non-failing heart. This is despite the desensitisation of the inotropic effect of isoprenaline in the same failing cells. Following beta-adrenoceptor stimulation, speeds of contraction and relaxation are normalised in myocytes from failing heart, with final values not significantly different from non-failing.
来自衰竭人类心室的心肌细胞的收缩和舒张比来自非衰竭心室的心肌细胞更缓慢。这被认为是由于衰竭心肌中基础环磷酸腺苷水平降低，以及随之而来的正性变松弛作用的减弱。我们通过证明β-肾上腺素能受体刺激对衰竭心脏的心肌细胞收缩和舒张的加速作用大于非衰竭心脏的心肌细胞，来提供数据支持这一假设。尽管在相同的衰竭细胞中异丙肾上腺素的正性肌力作用出现脱敏，但情况依然如此。在β-肾上腺素能受体刺激后，衰竭心脏的心肌细胞的收缩和舒张速度恢复正常，最终值与非衰竭心脏的心肌细胞无显著差异。
