No abstract

Overnight blood sampling for repeated growth hormone (GH) assays, regarded as the most physiological assessment of GH status, may induce some disturbances in patients’ sleep and then in the evaluation of GH secretion. We studied the influence of a hypnotic drug, zolpidem (10 mg), on nocturnal GH profiles (GH peak, time to first and maximum GH peak, area under the curve, mean integrated concentration) over two nights at a 7-day interval, in a double-blind cross-over design in a group of 12 young adult volunteers (27.9 ± 4.3 years), and in a group of 12 children (10.8 ± 2.3 years) with short stature, in a parallel double-blind study. Mean GH profiles showed no difference between zolpidem-treated subjects and placebo-treated controls, either in adults or in children. Although in these experimental conditions, sleep onset latency was significantly reduced with zolpidem in the adult volunteers, the mean time to first GH peak remained unchanged. Furthermore, GH profile did not relate with sleep duration, sleep onset latency or number of awakenings. A hypnotic drug, such as zolpidem, given at bedtime, is therefore devoided of effect on nocturnal GH profile and may be used in young children for overnight blood sampling when needed.

Because pituitary GH release is inhibited by GIH and hypothalamic secretion of this peptide seems to be mainly dependent on 8-adrenergic regulation,we have investigated if BAB could modify the pattern of GH response to GRF-29 in 5SN (3V,2F;7.8-9.6 y) and 5IGH-D (4M,lF;6.3-12.7).Blood samples for GH where collected from-15'to+ 60'according the following tests:' A)Propranolol(1 mg/kg,as iv bolus at-6O');B)GRF(l mcg/kg,as iv bo- .

No abstract

Growth hormone-releasing hormone, GHRH(l-44), was administered intranasally to 16 healthy young adult male volunteers in a placebo-controlled study using a dose of 1,000 µg dissolved in two different solvent vehicles: water alone and water with the surface tension-lowering agent Tween 80 (0.12%). The growth hormone (GH)-releasing effects of intranasal GHRH as well as that of the vehicle were established and compared to the effects of 80 µg intravenous GHRH. Plasma GH response was assessed by frequent blood sampling over an 180-min period, using both peak response and area under the curve (AUC). The results show that the GH-releasing effects of intranasal GHRH are comparable whichever vehicle is used, and are similar, with the dose of 1,000 µg, to the response obtained following the administration of 80 µg intravenous GHRH. Peak GH responses to GHRH (means ± SEM) were 25.6 ± 4.2 ng/ml (1,000 µg GHRH with water), 32.9 ± 9.1 ng/ml (1,000 µg with water plus Tween 80) and 36.3 ± 7.8 ng/ml (80 µg i.v. administration) (not significant). There was no significant GH response to placebo. Mean peak GH responses occurred after approximately 30 min in all three active treatments (29.2 ± 2.7, 33.9 ± 3.2 and 30.9 ± 3.9 min, respectively). The AUC values (ng·min· ml”1) were not statistically different: 1,914.4 ± 386.7 (water), 2,176.2 ± 599.9 (water plus Tween 80) and 2,419.2 ± 506.9 (i.v.) (not significant). Intranasal GHRH administration was well tolerated in all subjects. Occasional local reactions consisted of a prickly sensation in the nostrils or sneezing irrespective of the vehicle used. Long-term tolerance should be established before considering trial of intranasal GHRH administration in the treatment of GH-deficient children.