Angerås U, Hasselgren P O
Endocrinology. 1987 Apr;120(4):1417-21. doi: 10.1210/endo-120-4-1417.
beta-Blocking agents are increasingly used in the management of hyperthyroid patients. The effect of this treatment on increased muscle protein breakdown in the hyperthyroid state is not known. In the present study, experimental hyperthyroidism was induced in rats by daily ip injections of T3 (100 micrograms/100 g BW) during a 10-day period. Control animals received corresponding volumes of solvent. In groups of rats the selective beta-1-blocking agent metoprolol or the nonselective beta-blocker propranolol was infused by miniosmotic pumps implanted sc on the backs of the animals. Protein degradation was measured in incubated intact soleus and extensor digitorum longus muscles by determining tyrosine release into the incubation medium. The protein degradation rate in incubated extensor digitorum longus and soleus muscles was increased by 50-60% during T3 treatment. Metoprolol or propranolol did not influence muscle protein breakdown in either T3-treated or control animals. The results suggest that T3-induced increased muscle proteolysis is not mediated by beta-receptors, and muscle weakness and wasting in hyperthyroidism might not be affected by beta-blockers.
β受体阻滞剂在甲状腺功能亢进患者的治疗中应用越来越广泛。这种治疗方法对甲状腺功能亢进状态下肌肉蛋白质分解增加的影响尚不清楚。在本研究中，通过在10天内每天腹腔注射T3（100微克/100克体重）诱导大鼠实验性甲状腺功能亢进。对照动物注射相应体积的溶剂。在大鼠组中，通过植入动物背部皮下的微型渗透泵输注选择性β1受体阻滞剂美托洛尔或非选择性β受体阻滞剂普萘洛尔。通过测定酪氨酸释放到孵育培养基中的量，在孵育的完整比目鱼肌和趾长伸肌中测量蛋白质降解。在T3治疗期间，孵育的趾长伸肌和比目鱼肌中的蛋白质降解率增加了50-60%。美托洛尔或普萘洛尔对T3治疗的动物或对照动物的肌肉蛋白质分解均无影响。结果表明，T3诱导的肌肉蛋白水解增加不是由β受体介导的，甲状腺功能亢进时的肌肉无力和消瘦可能不受β受体阻滞剂的影响。
