Harding S E, Davia K, Davies C H, del Monte F, Money-Kyrle A R, Poole-Wilson P A
National Heart and Lung Institute, Imperial College School of Medicine, London, UK.
Ann Med. 1998 Aug;30 Suppl 1:14-23.
To determine whether there is a defect in the surviving muscle cells of the failing human heart, studies have been performed on individual myocytes isolated from normal and failing human myocardium. Myocytes from the failing ventricle contract and relax more slowly, and have a reduced contraction amplitude at physiological (but not low) stimulation frequencies. Slow relaxation is seen irrespective of the aetiology of the heart disease studied, and is more pronounced in myocytes from hypertrophied ventricles. Myocytes from hypertrophied ventricles are larger than normal, but the relaxation deficit is independent of cell size. Beta-adrenoceptor desensitization is evident in myocytes and it varies according to the severity of disease and with the age of the patient. Action potentials are longer in myocytes from failing human heart, probably because of an alteration in K+ current density. Many of the functional changes identified in failing human myocardium are seen at the level of the single cardiac myocyte, which implies that pharmacological or genetic manipulation of surviving cells is a logical therapeutic strategy.
为了确定衰竭的人类心脏中存活的心肌细胞是否存在缺陷，已对从正常和衰竭的人类心肌中分离出的单个心肌细胞进行了研究。来自衰竭心室的心肌细胞收缩和舒张更缓慢，并且在生理（而非低）刺激频率下收缩幅度降低。无论所研究的心脏病病因如何，均可观察到舒张缓慢，并且在肥厚心室的心肌细胞中更为明显。肥厚心室的心肌细胞比正常细胞大，但舒张缺陷与细胞大小无关。β-肾上腺素能受体脱敏在心肌细胞中很明显，并且它根据疾病的严重程度和患者的年龄而变化。来自衰竭人类心脏的心肌细胞动作电位更长，这可能是由于钾电流密度的改变。在衰竭的人类心肌中发现的许多功能变化在单个心肌细胞水平上即可观察到，这意味着对存活细胞进行药理学或基因操作是一种合理的治疗策略。
