Porta S, Emsenhuber W, Felsner P, Schauenstein K, Supanz S
Institute of Functional Pathology, University of Graz, Austria.
Life Sci. 1989;45(19):1763-9. doi: 10.1016/0024-3205(89)90515-8.
Our experiments did show that chronic 12 hours administration of norepinephrine (NE) to rats by means of subcutaneously implantable retard tablets, led to a highly significant epinephrine (E) depletion of the adrenal medulla during normoglycemia. The expected rise of free plasma NE at 6 and 12 hours was accompanied by increased free plasma E values at 12 hours. At this very time point the liver contents of glycogen and free intracellular glucose showed their most pronounced decrease. Since at 12 hours both liver glycogen and medullar E values were at their lowest, a second experiment was performed to examine a possible causal relationship. In order to curb the breakdown of liver glycogen, rats were force fed with 50% glucose solution 9 hours after NE tablet implantation. Glucose feeding not only caused a much less pronounced liver glycogen fall at 12 hours, but, at the same time also prevented E depletion of the adrenal medulla. These observations suggested that rapid fall of liver glycogen and/or liver intracellular free glucose might be the trigger for medullar E depletion, even before hypoglycemia.
我们的实验确实表明，通过皮下植入缓释片对大鼠进行12小时的去甲肾上腺素（NE）慢性给药，会导致正常血糖期间肾上腺髓质的肾上腺素（E）显著耗竭。在6小时和12小时时，游离血浆NE预期的升高伴随着12小时时游离血浆E值的增加。就在这个时间点，肝脏糖原和细胞内游离葡萄糖的含量出现了最明显的下降。由于在12小时时肝脏糖原和髓质E值均处于最低水平，因此进行了第二项实验以研究可能的因果关系。为了抑制肝糖原的分解，在植入NE片9小时后，给大鼠强制喂食50%的葡萄糖溶液。葡萄糖喂食不仅在12小时时导致肝糖原下降的程度明显减轻，而且同时还防止了肾上腺髓质的E耗竭。这些观察结果表明，肝糖原和/或肝脏细胞内游离葡萄糖的快速下降可能是髓质E耗竭的触发因素，甚至在低血糖之前。
