地塞米松诱发肌病的组织学和组织化学研究

HISTOLOGICAL AND HISTOCHEMICAL STUDY OF DEXAMETHASONE INDUCED MYOPATHY

36只兔分2组,分别肌注0.5mg/kg和1.5mg/kg剂量的地塞米松14d、2Sd和42d。另12只兔注盐水对照,用H.E、琥珀酸脱氢酶、胆碱酯酶法浸染比目鱼肌、趾长伸肌和胫骨前肌,用光镜及电镜观察,并用微机处理。结果表明,地塞米松诱发肌病,肌纤维肿胀、萎缩、坏死、体重降低。长期常规用药与短期大剂量用药具有同等负效应。病变主要累及白肌纤维,其机制可能是对肌酵解酶和运动终板胆碱酯酶的共同抑制及直接影响肌纤维蛋白质的合成。

Dexamethasone in dose of 0. 5mg/kg and 1.5 mg/kg were intramuscularlyinjected respectively for 14, 28 and 42 days in 36 rabbits divided inio twogroups. The other 12 control animals were treated with saline injections. Thesoleus, extensor digitorum longus and tibialis anterior were stained with H.E.,succino-dehydrogenase, and acetylcholinesterase and examined by electronic mic-roscope. Myopathy induced by dexamethasone represented swelling, atrophy andnecrosis of muscle fibers. The routine dose of dexamethasone for a long periodand large dose for a short period caused the same negative effect.The myopathyoccured mainly in white muscle fibres. Its mechanism was probably that therole of glucccorticoid resulted in an inhibition of glucolyases and acetylcholine-sterases, and in a suppression of the synthesis of protein.