Vermes I, Beishuizen A, Hampsink R M, Haanen C
Department of Clinical Chemistry, Medical Spectrum Twente, Enschede, The Netherlands.
J Clin Endocrinol Metab. 1995 Apr;80(4):1238-42. doi: 10.1210/jcem.80.4.7714094.
The regulatory mechanisms of the hypothalamo-pituitary-adrenal system were studied in critically ill, intensive care unit patients. Serial measurements of immunoreactive ACTH-(1-39) (ACTHi), cortisol, endothelin-1 (ETi), and atrial natriuretic hormone (ANHi) were performed in blood samples of 18 patients with clinically defined sepsis, 12 critically ill patients after multiple trauma, and 15 hospitalized matched control subjects without acute illness for 8 consecutive days after admission. On admission, plasma levels of cortisol and ACTHi were significantly elevated in patients with sepsis (1.32 +/- 0.21 mumol/L and 130.0 +/- 38.2 pmol/L, mean +/- SD) and with multiple trauma (1.23 +/- 0.28 mumol/L and 123.7 +/- 41.3 pmol/L) compared to those in the control subjects (0.37 +/- 0.08 mumol/L and 15.6 +/- 5.8 pmol/L, respectively). The plasma cortisol levels of critically ill patients remained high (> 0.8 mumol/L) during the whole observation period. In contrast, plasma ACTHi levels decreased between days 3-5, reaching significantly lower levels on day 5 compared to those in the control group and remained below 5.0 pmol/L during the rest of the observation period. Plasma levels of ETi and ANHi were significantly elevated during the whole period in both patient groups (ETi, > 10 ng/L; ANHi, > 250 ng/L) compared to those in control subjects (< 5 and < 50 ng/L, respectively). The high plasma concentration of ETi observed in our patients may stimulate the steroid secretion of the adrenal cortex directly or potentiate the adrenal effect of ACTH. On the other hand, the increased concentration of ANHi found in critically ill patients together with the increased plasma cortisol level may explain the inhibition of ACTH secretion. Accordingly, we speculate that the high ET level exerts a positive drive on the adrenocortical level, that the high ANH level has an inhibitory effect on the hypothalamo-pituitary level, and that both mechanisms play a role in regulation of the hypothalamo-pituitary-adrenal axis during critical illness.
对重症监护病房的危重症患者下丘脑 - 垂体 - 肾上腺系统的调节机制进行了研究。对18例临床诊断为脓毒症的患者、12例多发伤危重症患者以及15例无急性疾病的住院对照受试者的血样连续8天进行免疫反应性促肾上腺皮质激素（1 - 39）（ACTHi）、皮质醇、内皮素 - 1（ETi）和心房利钠肽（ANHi）的测定。入院时，脓毒症患者（1.32±0.21μmol/L和130.0±38.2pmol/L，均值±标准差）和多发伤患者（1.23±0.28μmol/L和123.7±41.3pmol/L）的血浆皮质醇和ACTHi水平与对照受试者（分别为0.37±0.08μmol/L和15.6±5.8pmol/L）相比显著升高。危重症患者的血浆皮质醇水平在整个观察期内一直保持较高（>0.8μmol/L）。相比之下，血浆ACTHi水平在第3 - 5天下降，与对照组相比，第5天显著降低，并在观察期剩余时间内保持在5.0pmol/L以下。与对照受试者（分别<5和<50ng/L）相比，两组患者在整个观察期内血浆ETi和ANHi水平均显著升高（ETi，>10ng/L；ANHi，>250ng/L）。在我们的患者中观察到的高血浆ETi浓度可能直接刺激肾上腺皮质的类固醇分泌或增强ACTH对肾上腺的作用。另一方面，危重症患者中发现的ANHi浓度增加以及血浆皮质醇水平升高可能解释了ACTH分泌的抑制。因此，我们推测高ET水平对肾上腺皮质水平产生正向驱动作用，高ANH水平对下丘脑 - 垂体水平具有抑制作用，并且这两种机制在危重症期间下丘脑 - 垂体 - 肾上腺轴的调节中均发挥作用。
