Lännergren J, Westerblad H, Flock B
Department of Physiology II, Karolinska Institutet, Stockholm, Sweden.
Acta Physiol Scand. 1990 Nov;140(3):437-45. doi: 10.1111/j.1748-1716.1990.tb09019.x.
In the preceding paper we showed that post-contractile depression is accompanied by an increased light scattering in the light microscope, which suggests an association between morphological changes and the force reduction. In the present paper the morphology of fatigued fibres has been studied using electron microscopical techniques. Fibres fixed in glutaraldehyde during maximum post-contractile depression (about 20 min after fatiguing stimulation) contained a large number of vacuoles. Fibres fixed earlier displayed generally swollen and in some cases vesiculated mitochondria, but only a few vacuoles. Fixation methods aiming at visualizing the T-tubular system revealed apparent communications between T-tubules and vacuoles; apart from this the T-tubular system, as well as the triadic junctions, appeared to be normal. We consider it most likely that the vacuoles primarily originate from damaged mitochondria, but other possibilities cannot be excluded. Further, a simple causal relation between the observed ultrastructural changes and the force depression is not obvious. Rather we suggest that post-contractile depression is caused by additional changes in the triadic junctions, which were not detected with the present techniques.
在前一篇论文中,我们指出收缩后抑制伴随着光学显微镜下光散射的增加,这表明形态学变化与力的降低之间存在关联。在本文中,我们使用电子显微镜技术研究了疲劳纤维的形态。在最大收缩后抑制(疲劳刺激后约20分钟)期间用戊二醛固定的纤维含有大量液泡。较早固定的纤维通常显示线粒体肿胀,在某些情况下呈泡状,但只有少数液泡。旨在观察T小管系统的固定方法显示T小管与液泡之间存在明显的连通;除此之外,T小管系统以及三联体连接似乎是正常的。我们认为液泡最有可能主要源自受损的线粒体,但其他可能性也不能排除。此外,观察到的超微结构变化与力的降低之间的简单因果关系并不明显。相反,我们认为收缩后抑制是由三联体连接的其他变化引起的,而目前的技术未检测到这些变化。