Opie L H, Walpoth B, Barsacchi R
J Mol Cell Cardiol. 1985 Jul;17 Suppl 2:21-34. doi: 10.1016/0022-2828(85)90005-7.
There are marked differences between human cardiomyopathies, especially of the hypertrophic variety, and animal models. There is no simple way in which a hyperadrenergic state can explain the contractile abnormalities, although additional effects of calcium overload or marked hypertrophy come somewhat closer to linking animal and human diseases. One of the best links between excess catecholamine stimulation and myocardial damage lies in the enhanced sarcolemmal permeability which is mediated by beta-adrenergic stimulation and calcium ions in an isolated rat heart model. The therapeutic success of beta-adrenergic blockade and especially calcium antagonists in no way provide firm evidence for a hyperadrenergic state nor for intracellular calcium overload. In human hypertrophic cardiomyopathy, these agents may be acting merely by enlarging cavity size. In dilated cardiomyopathy, the use of beta-adrenergic blockers is still highly controversial and calcium antagonists are not well tested. It is the lack of appropriate models for both hypertrophic cardiomyopathy and dilated cardiomyopathy which is holding up research in this important area.
人类心肌病，尤其是肥厚型心肌病，与动物模型之间存在显著差异。尽管钙超载或明显肥大的额外影响在一定程度上更接近于将动物疾病和人类疾病联系起来，但高肾上腺素能状态并没有简单的方式来解释收缩异常。在离体大鼠心脏模型中，过量儿茶酚胺刺激与心肌损伤之间的最佳联系之一在于由β-肾上腺素能刺激和钙离子介导的肌膜通透性增强。β-肾上腺素能阻滞剂尤其是钙拮抗剂的治疗成功并不能为高肾上腺素能状态或细胞内钙超载提供确凿证据。在人类肥厚型心肌病中，这些药物可能仅仅是通过扩大腔室大小起作用。在扩张型心肌病中，β-肾上腺素能阻滞剂的使用仍然存在很大争议，而钙拮抗剂尚未得到充分测试。正是由于缺乏适用于肥厚型心肌病和扩张型心肌病的模型，阻碍了这一重要领域的研究。
