Porta S, Egger G, Sadjak A, Supanz S, Rangetiner B, Pürstner P
Exp Pathol. 1984;25(3):169-76. doi: 10.1016/s0232-1513(84)80036-5.
In a frequently cited paper Sokal , Sarcione and Henderson (1964) doubted the physiological glycogenolytic role of adrenaline (A). By using isolated perfused rat livers, they found adrenaline to be effective at doses higher than 140 ng/ml while a mere tenfold increase in glucagon leads to expressed glycogenolysis. Our in vivo experiments carried out with controlled release systems for adrenaline show that marked glycogenolysis takes place at an adrenaline serum level of not more than 20 ng/ml while endogenous glucagon levels do not differ from controls. We think, that the reason for those controversial results lies in the fact that Sokal , Sarcione and Henderson (1964) diminished the glycogenolytic action of adrenaline by blocking its alpha-component for the reason of an easier perfusion, and they further diminished its glycogenolytic action by omitting corticosterone, which is well known for its permissive role in adrenaline induced glycogenolysis in vivo.
在一篇被频繁引用的论文中，索卡尔、萨乔内和亨德森（1964年）对肾上腺素（A）的生理性糖原分解作用表示怀疑。通过使用离体灌注大鼠肝脏，他们发现肾上腺素在剂量高于140纳克/毫升时才有效，而胰高血糖素仅增加十倍就能导致明显的糖原分解。我们使用肾上腺素控释系统进行的体内实验表明，在肾上腺素血清水平不超过20纳克/毫升时就会发生明显的糖原分解，而内源性胰高血糖素水平与对照组无差异。我们认为，这些有争议结果的原因在于，索卡尔、萨乔内和亨德森（1964年）为了便于灌注而阻断肾上腺素的α成分，从而削弱了肾上腺素的糖原分解作用，并且他们进一步通过省略皮质酮来削弱其糖原分解作用，而皮质酮在体内肾上腺素诱导的糖原分解中具有众所周知的允许作用。
