棉酚对动物腓肠肌影响的电子显微镜观察

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本文报道了醋酸棉酚对雄猴、大鼠和豚鼠腓肠肌超微结构的影响。雄性恒河猴按4毫克/公斤/日服棉酚两年,其腓肠肌超微结构基本保持正常。但个别动物腓肠肌肌细胞核出现固缩和核膜分离。成年 Wistar 雄性大鼠服抗生育剂量棉酚(20、30毫克/公斤/日×30)时,除光滑内质网轻度扩张及核膜分离外,腓肠肌超微结构与对照比较无明显变化。豚鼠实验亦得到类似结果。大鼠服棉酚剂量加大到(60毫克/公斤/日×37)时,虽然大部分肌原纤维仍保持正常的周期性结构,可见递次重复的明带和暗带。但某些肌原纤维失去正常纹理,有的Ⅰ带明显加宽,还有少数肌原纤维开始断裂、溶解,而线粒体未见明显病变。当大鼠服药时间延长至55日时,上述病变更加明显。线粒体细长,排列紊乱,同时更多的肌原纤维出现萎缩和断裂,表现为原纤维型坏死。豚鼠口服棉酚(60毫克/公斤/日×25)时,肌原纤维变化不甚明显,而部分线粒体出现不同程度的肿胀变性,损伤严重的线粒体嵴断裂溶解,表现为线粒体型坏死。本文初步分析和讨论了以上结果与低钾性肌无力的关系。 This paper reports the effect of gossypol acetate on the ultrastructure of gastrocnemius muscle in male monkeys, rats and guinea pigs. Male rhesus monkeys were given gossypol at 4 mg/kg/day for two years, and their ultrastructure of the gastrocnemius muscles remained normal. However, pneumonia and nuclear membrane separation occur in the nuclei of gastrocnemius muscle in some animals. When adult Wistar male rats were given anti-fertility dose of gossypol (20, 30 mg/kg/day × 30), there was no significant change in the ultrastructure of gastrocnemius muscle compared with controls except for the mild expansion of the smooth endoplasmic reticulum and nuclear membrane separation. Guinea pig experiments also gave similar results. When the dose of gossypol in rats was increased (60 mg/kg/day×37), although most myofibrils still maintained a normal periodic structure, repeated bands and dark bands were seen. However, some myofibrils have lost their normal texture. Some I bands have been significantly widened, and a few myofibrils have begun to break and dissolve, but no obvious lesions have been seen in mitochondria. When the time taken by the rats was extended to 55 days, the above lesions were more pronounced. The mitochondria are slender and disorganized, and more myofibrils are atrophied and broken, showing fibrillar necrosis. When guinea pigs were treated with gossypol (60 mg/kg/day×25), myofibrils did not change significantly, and some mitochondria showed varying degree of swelling and degeneration. Severely damaged mitochondria were broken and dissolved, showing mitochondrial necrosis. This article primarily analyzes and discusses the relationship between the above results and hypokalemic muscle weakness.
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