纳络酮对正常人和Cushing病患者胰岛素低血糖兴奋后ACTH分泌的影响

EFFECT OF NALOXONE ON THE SECRETION OF ACTH AND CORTISOL STIMULATED BY INSULIN-INDUCED HYPOGLYCEMIA IN NORMAL SUBJECTS AND PATIENTS WITH CUSHING'S DISEASE

以血清N-POMC水平作为ACTH分泌的指标,观察了纳络酮(25mg)对5例正常人和5例Cushing病患者胰岛素低血糖兴奋后ACTH和皮质醇(F)分泌的影响,发现正常人胰岛素低血糖试验血N-POMC和F水平明显升高;加用类阿片肽受体阻滞剂纳络酮不能使胰岛素低血糖试验时血N-POMC和F的上升幅度进一步增加。推测这两种刺激兴奋CRH的途径相似,提示胰岛素低血糖试验可能涉及到类阿片肽机制。对Cushing病患者,无论是单纯胰岛素低血糖还是胰岛素低血糖加纳络酮均不能改变其血N-POMC和F水平,可能此两种刺激均未能引起内源性CRH释放增加。

The effect of naloxone (25 mg) on the release of AGTH and cortisol stimulated by insulin-induced hypoglycemia in five normal subjects and five patients with Cushing's disease was studied. Serum N-POMC level was used as indication of ACTH secretion. In normal subjects, insulin-induced hypoglycemia (RI 0.15 U / kg) caused prompt increases in blood N-POMC and cortisol levels. The peak values of N-POMC and cortisol during insulin-induced hypoglycemia were 75.5±12.4 pmol/L and 897.2±66.3 nmol /L respectivelyj which were unchanged by the additional injection of naloxone. The effects of naloxone and insulin were not additive-These results indicate that the release of ACTH stimulated by naloxone or the hypoglycemia-stress may act, at least in part, through common mechanisms, that is, through deletion of opiate inhibition on pituitary-adrenal axis. But in the patients with Cushing's disease, both insulin-induced hypoglycemia (RI 0.30 U / kg) and naloxone could not alter the blood N-POMC and cortisol levels.