长效肾上腺素胶囊对低血糖大鼠肾上腺素消耗的抑制作用

S. Porta, G. Egger, R. Kubat, R. Sattelberger
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引用次数: 4

摘要

通过皮下储存胶囊(含40毫克干肾上腺素/盐酸,默克,10毫克抗坏血酸和0.4毫升0.9%氯化钠,并用透析膜密封以提供恒定的肾上腺素输出)对大鼠进行肾上腺素慢性治疗,可导致原发性高血糖期后进入低血糖。低血糖发作时,肾上腺素含量降至正常水平的三分之一左右。同时腹腔内滴注葡萄糖可预防低血糖和肾上腺素耗竭。肾上腺素的消耗并不总是与血糖水平低于80毫克/分升相对应,这种消耗可以通过葡萄糖输注完全阻止,这一事实似乎提供了一个强烈的暗示,即上述消耗是由于肾上腺素分泌过多,而不是由于肾上腺素合成受阻。如果是真的,那么在肾上腺素分泌和它的腺外水平之间一定没有直接的负反馈系统。
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Inhibition of adrenalin depletion in hypoglycaemic rats following permanent adrenalin application by depot capsule

Chronic treatment of rats with adrenalin by means of a subcutaneous depot capsule (cont. 40 mg dry adrenalin/HCl, Merck, ca. 10 mg ascorbic acid and ca. 0.4 ml 0.9 % NaCl, and sealed with a dialysis membrane to provide constant adrenalin output) leads after a primary hyperglycaemic phase to hypoglycaemia. At the onset of hypoglycaemia the adrenalin contents of the suprarenal glands decrease to levels of about one third of their normal state. Simultaneous glucose infusions by intraperitoneal depot capsules prevent hypoglycaemia as well as adrenalin depletion.

The fact that adrenalin depletion does not always correspond with blood sugar levels below 80 mg/dl and that this depletion could be prevented by glucose infusions altogether seems to provide a strong hint that the mentioned depletion is due to hypersecretion and not to the blocking of adrenalin synthesis.

If is true, then there must be no direct negative feed-back system between adrenalin secretion and its extraglandular level.

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