Møller J, Frandsen E, Fisker S, Jørgensen J O, Christiansen J S
Medical Department M, Aarhus Kommunehospital, Denmark.
Clin Endocrinol (Oxf). 1996 May;44(5):533-9. doi: 10.1046/j.1365-2265.1996.728550.x.
There are few data on the endocrine mechanisms underlying the body fluid changes in GH deficiency and their subsequent alteration following GH replacement. We have therefore investigated the time effects of GH on body fluid distribution and fluid regulating hormones in GH deficient adults.
The patients underwent in random order four study periods: (1) saline, a 42-hour infusion following 3 weeks without GH, (2) acute GH, a 42-hour GH infusion following 3 weeks without GH, (3) 3 days GH, a 42-hour GH infusion preceded by 3 weeks without GH and 3 days pretreatment with subcutaneous GH injections, (4) 3 weeks GH, a 42-hour GH infusion after at least 3 weeks GH therapy.
Seven GH deficient adult males and 8 healthy control subjects.
During each infusion period 24-hour blood pressure was recorded, bioimpedance was repeatedly measured and blood samples were obtained every 6 hours. After 41 hours extracellular and plasma volumes were determined isotopically. Extracellular volume, plasma volume and bioimpedance were measured in the control group.
GH increased extracellular volume (saline 16.45 +/- 0.79 vs acute GH 16.83 +/- 0.87; vs 3 days GH 17.58 +/- 0.71; vs 3 weeks GH 17.92 +/- 0.88 l, P = 0.01). After 3 weeks of GH, extracellular volumes in the patients and in the control group were identical (control 17.94 +/- 0.32). Plasma volume was increased only after 3 weeks GH treatment (saline 2.93 +/- 0.16 vs acute GH 3.04 +/- 0.22; vs 3 days GH 3.06 +/- 0.07; vs 3 weeks GH 3.37 +/- 0.18 l, P = 0.03), and was decreased compared to the control group (control 3.56 +/- 0.03 l, P < 0.01). Bioimpedance decreased significantly in all treatment periods and was significantly increased compared to the control group. Plasma renin increased during GH administration (saline 16.2 +/- 1.9 vs acute 19.0 +/- 1.9; vs 3 days GH 30.8 +/- 3.0; vs 3 weeks GH 27.0 +/- 3.0 mU/l, P = 0.03), whereas aldosterone and atrial natriuretic factor (ANF) levels remained unaffected by GH. GH caused an increase in systolic blood pressure (BP) and heart rate, whereas diastolic BP remained unaffected.
The present data show that GH deficiency is associated with decreased plasma volume and extracellular volume. GH exposure acutely increases extracellular volume, whereas substitution for a longer time was required to normalize both extracellular and plasma volumes. Renin seems to be involved in these fluid volume regulating effects of GH.
关于生长激素缺乏症患者体液变化的内分泌机制及其生长激素替代治疗后的后续改变的数据较少。因此,我们研究了生长激素对生长激素缺乏的成年人的体液分布和体液调节激素的时间效应。
患者按随机顺序接受四个研究阶段:(1)生理盐水阶段,在停用生长激素3周后进行42小时的生理盐水输注;(2)急性生长激素阶段,在停用生长激素3周后进行42小时的生长激素输注;(3)3天生长激素阶段,在停用生长激素3周后进行42小时的生长激素输注,之前3天进行皮下生长激素注射预处理;(4)3周生长激素阶段,在至少3周生长激素治疗后进行42小时的生长激素输注。
7名生长激素缺乏的成年男性和8名健康对照者。
在每个输注阶段记录24小时血压,反复测量生物电阻抗,并每6小时采集血样。41小时后通过同位素法测定细胞外液和血浆容量。对照组测量细胞外液容量、血浆容量和生物电阻抗。
生长激素增加细胞外液容量(生理盐水组16.45±0.79 vs急性生长激素组16.83±0.87;vs 3天生长激素组17.58±0.71;vs 3周生长激素组17.92±0.88升,P = 0.01)。生长激素治疗3周后,患者和对照组的细胞外液容量相同(对照组17.94±0.32)。仅在生长激素治疗3周后血浆容量增加(生理盐水组2.93±0.16 vs急性生长激素组3.04±0.22;vs 3天生长激素组3.06±0.07;vs 3周生长激素组3.37±0.18升,P = 0.03),且与对照组相比降低(对照组3.56±0.03升,P < 0.01)。在所有治疗阶段生物电阻抗均显著降低,且与对照组相比显著升高。生长激素给药期间血浆肾素增加(生理盐水组16.2±1.9 vs急性生长激素组19.0±1.9;vs 3天生长激素组30.8±3.0;vs 3周生长激素组27.0±3.0 mU/l,P = 0.03),而醛固酮和心房利钠因子(ANF)水平不受生长激素影响。生长激素导致收缩压(BP)和心率升高,而舒张压不受影响。
目前的数据表明,生长激素缺乏与血浆容量和细胞外液容量降低有关。生长激素暴露可急性增加细胞外液容量,而需要较长时间的替代治疗才能使细胞外液和血浆容量恢复正常。肾素似乎参与了生长激素对这些体液容量的调节作用。