Miller J L, Ismail F, Waligora J K, Gevers W
Endocrinology. 1985 Sep;117(3):869-71. doi: 10.1210/endo-117-3-869.
There is evidence suggesting that thyrotoxicosis increases beta-adrenoreceptor density on some target tissues. We have studied the in vivo effect of D,L-propranolol (a nonselective beta-adrenoreceptor blocking agent) on T3-induced enhancement of in situ proteolysis in fast twitch muscle fibers of the rat. Chronic treatment with T3 as opposed to saline resulted in a 76% enhancement of the rate of in situ muscle proteolysis [0.79 +/- 0.04 (n = 8) compared with 0.45 +/- 0.01 (n = 8) nmol tyrosine/mg muscle . 2 h]. Treatment of rats with both T3 and 2 mg propranolol resulted in a 62% reduction in the T3-induced increment in situ muscle proteolysis [0.58 +/- 0.02 (n = 8) vs. 0.79 +/- 0.04]. This significant inhibition by propranolol of T3-induced enhanced proteolytic rates in vitro suggests that this may comprise one component of the observed beneficial clinical effects of beta-blockade in thyrotoxic myopathy.
有证据表明，甲状腺毒症会增加某些靶组织上的β-肾上腺素能受体密度。我们研究了D，L-普萘洛尔（一种非选择性β-肾上腺素能受体阻滞剂）对T3诱导的大鼠快肌纤维原位蛋白水解增强的体内作用。与生理盐水相比，用T3进行慢性治疗导致原位肌肉蛋白水解速率提高了76%[0.79±0.04（n = 8），而0.45±0.01（n = 8）nmol酪氨酸/毫克肌肉·2小时]。用T3和2毫克普萘洛尔同时治疗大鼠，可使T3诱导的原位肌肉蛋白水解增加减少62%[0.58±0.02（n = 8）对0.79±0.04]。普萘洛尔对T3诱导的体外蛋白水解速率增强的这种显著抑制作用表明，这可能是β受体阻滞剂在甲状腺毒症性肌病中观察到的有益临床效果的一个组成部分。
