Munsat T L, Hudgson P, Johnson M A
Neurology. 1977 Aug;27(8):772-82. doi: 10.1212/wnl.27.8.772.
One hundred and eight Wistar rats were injected with serotonin (20 mg per kilogram of body weight intraperitoneally) or imipramine hydrochloride (20 mg per kilogram intraperitoneally), or both, in a single cycle or in multiple (up to 18 weeks) weekly cycles. In contrast to previous reports, a characteristic myopathy was produced with serotonin alone, identical to that produced by serotonin and imipramine in combination. Imipramine alone produced no significant change. The myopathy produced was characterized by (1) preferential damage to myofibers with high oxidative capacity (types I and IIA), (2) prominent regenerative activity occurring as early as 48 hours, and (3) degeneratio of capillary endothelium (thickening, vacuolar degeneration, proliferation of marginal folds, dissolution of mitochondria). Small groups of degenerating fibers and increased connective tissue were not observed. There was no loss of myofibers or fat replacement. The changes suggested repeated acute insults followed the complete recovery. These observations suggest that although the pathogenesis of serotonin and serotonin-imipramine myopathy is primarily ischemic, it is not a satisfactory model of human Duchenne muscular dystrophy.
108只Wistar大鼠被腹腔注射血清素（每千克体重20毫克）或盐酸丙咪嗪（每千克20毫克腹腔注射），或两者同时注射，单次注射或每周多次（长达18周）循环注射。与之前的报道不同，单独使用血清素会产生一种特征性肌病，与血清素和丙咪嗪联合使用产生的肌病相同。单独使用丙咪嗪未产生显著变化。所产生的肌病的特征为：（1）优先损伤具有高氧化能力的肌纤维（I型和IIA型）；（2）早在48小时就出现显著的再生活动；（3）毛细血管内皮变性（增厚、空泡变性、边缘褶皱增殖、线粒体溶解）。未观察到小群变性纤维和结缔组织增加。没有肌纤维丢失或脂肪替代。这些变化表明反复急性损伤后完全恢复。这些观察结果表明，尽管血清素和血清素 - 丙咪嗪肌病的发病机制主要是缺血性的，但它并不是人类杜兴氏肌营养不良症的理想模型。
