Krippendorf B B, Riley D A
Department of Cellular Biology and Anatomy, Medical College of Wisconsin, Milwaukee 53226.
Anat Rec. 1994 Mar;238(3):304-10. doi: 10.1002/ar.1092380304.
Focal sarcomere disruptions were previously observed in adductor longus muscles of rats flown approximately two weeks aboard the Cosmos 1887 and 2044 biosatellite flights. These lesions, characterized by breakage and loss of myofilaments and Z-line streaming, resembled damage induced by unaccustomed exercise that includes eccentric contractions in which muscles lengthen as they develop tension. We hypothesized that sarcomere lesions in atrophied muscles of space flow rats were not produced in microgravity by muscle unloading but resulted from muscle reloading upon re-exposure to terrestrial gravity. To test this hypothesis, we examined temporal changes in sarcomere integrity of adductor longus muscles from rats subjected to 12.5 days of hindlimb suspension unloading and subsequent reloading by return to vivarium cages for 0, 6, 12, or 48 hours of normal weightbearing. Our ultrastructural observations suggested that muscle unloading (0 h reloading) induced myofibril misalignment associated with myofiber atrophy. Muscle reloading for 6 hours induced focal sarcomere lesions in which cross striations were abnormally widened. Such lesions were electron lucent due to extensive myofilament loss. Lesions in reloaded muscles showed rapid restructuring. By 12 hours of reloading, lesions were moderately stained foci and by 48 hours darkly stained foci in which the pattern of cross striations was indistinct at the light and electron microscopic levels. These lesions were spanned by Z-line-like electron dense filamentous material. Our findings suggest a new role for Z-line streaming in lesion restructuring: rather than an antecedent to damage, this type of Z-line streaming may be indicative of rapid, early sarcomere repair.
先前在搭乘宇宙 1887 号和 2044 号生物卫星飞行约两周的大鼠内收长肌中观察到局灶性肌节破坏。这些病变的特征是肌丝断裂和丢失以及 Z 线流,类似于不习惯运动(包括离心收缩,即肌肉在产生张力时延长)所诱导的损伤。我们假设,太空飞行大鼠萎缩肌肉中的肌节病变不是由微重力下的肌肉卸载产生的,而是由于重新暴露于地球重力时的肌肉再加载所致。为了验证这一假设,我们检查了经历 12.5 天后肢悬吊卸载并随后通过返回饲养笼正常负重 0、6、12 或 48 小时进行再加载的大鼠内收长肌肌节完整性的时间变化。我们的超微结构观察表明,肌肉卸载(0 小时再加载)诱导了与肌纤维萎缩相关的肌原纤维排列不齐。肌肉再加载 6 小时诱导了局灶性肌节病变,其中横纹异常增宽。由于广泛的肌丝丢失,这些病变呈电子透明状。再加载肌肉中的病变显示出快速重塑。再加载 12 小时时,病变为中度染色灶,到 48 小时时为深色染色灶,在光镜和电镜水平上横纹图案均不清晰。这些病变被 Z 线样电子致密丝状物质跨越。我们的研究结果表明 Z 线流在病变重塑中具有新作用:这种类型的 Z 线流可能不是损伤的先兆,而是快速、早期肌节修复的指示,而不是损伤的先兆。