摘要
本研究旨在阐明呼吸肌在心肌病中的变化及其机制。研究了10只患有特发性扩张型心肌病(CM)的仓鼠和10只对照组,观察了膈肌的收缩特性和组织学,以及血清胰岛素样生长因子(IGF)-1水平。28周时,CM组的体重较对照组减少(114+/-10 g vs 144+/-14 g, p<0.0001)。CM组的膈肌与体重之比显著高于对照组(0.228+/-0.015 vs 0.182+/-0.017, p<0.0001)。体外实验发现,最大膈肌抽动(303+/-63 vs 455+/-119 g x cm(-2))和破板张力(1555 +/-369 vs 2204 +/-506 g x cm(-2))在cm组显著低于对照组(p<0.005)。半松弛时间在CM (19+/-1 ms)中显著短于对照组(24+/-3 ms, p<0.0005)。CM在25hz时的疲劳性(28%)显著低于对照组(42%,p<0.0001)。膈肌和腓肠肌腺苷三磷酸酶染色显示CM中I型纤维萎缩,与膈肌中I型纤维数量增加相关。两个肌肉的组织学检查显示异常的肌肉模式。最后,CM组血清IGF-1水平比对照组低47% (p<0.0001),且与膈肌收缩特性和组织学的变化明显相关。 In conclusion, cardiomyopathy in hamsters: 1) depressed the force-generating capacity and shortened the relaxation of the hamster diaphragm; 2) induced type I fibre atrophy in combination with a myopathic pattern; and 3) was associated with a significant reduction in serum levels of insulin-like growth factor-1, related to the diaphragmatic changes. Whether these changes are primary myopathic or secondary to heart failure remains to be elucidated.