Effects of convulsive electroshock on serum concentrations of follicle stimulating hormone, luteinizing hormone, thyroid stimulating hormone and growth hormone in man,.
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In patients with acromegaly whose basal plasma GH levels were suppressed with 9 mg/day of dexamethasone for 2 days, TRH-(6 cases) and LHRH-(1 case) induced GH release were unaffected when the responses were compared to the basal levels. Phentolamine infusion, 70 mg in 150 min, or hyperglycemia induced by iv infusion of 700 ml of 50% glucose solution also did not suppress TRH-induced GH release in 2 acromegalic patients whose basal GH levels were lowered with these agents alone. These results seem to indicate that dexamethasone does not affect TRH- or LHRH-induced GH release per se, but affects the basal state which determines the absolute level of response. They also support the concept that TRH and LHRH act directly on pituitary tumor cells to release GH in acromegaly.
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Three-weeks ovariectomized rats were sc implanted with Alzet osmotic minipumps which released either LRH or the LRH-analogue buserelin at the rate of 250 ng/h. Control rats were implanted with a silastic 'shampump'. After explantation, 6 days later, the pituitary glands of part of these rats were exposed to the maximally active LRH concentration of 1 micrograms/ml for a period of 6 h, using a perifusion system. In a second group of rats explantation and perifusion was done not directly, but 5 days after cessation of the LRH pre-treatment. After 6 days in vivo pre-treatment with LRH or with buserelin the pituitary LH and FSH stores were partially depleted, the depletion after buserelin being stronger than after LRH. The pituitary glands of the first group of rats showed rates of both maximally LRH-stimulated and unstimulated (autonomous) LH- and FSH-secretion which were strongly impaired, the impairment after buserelin being stronger than after LRH. In the group with a 5 days interval between in vivo LRH/buserelin pre-treatment and explantation the pituitary LH and FSH stores were restored to the range of pre-treatment levels. Of these pituitaries the autonomous secretion of LH and FSH as well as the maximally LRH-stimulated secretion of FSH was restored to the normal level; the maximally LRH-stimulated secretion of LH, however, remained depressed, indicating that 5 days after cessation of exposure to LRH or to buserelin, and in spite of restored pituitary LH/FSH contents, the sensitivity of the LH releasing system to LRH was still subnormal.(ABSTRACT TRUNCATED AT 250 WORDS)
We evaluated the effects of iv pretreatment with exogenous GH on the GH response to GHRH either alone or in combination with pyridostigmine in 14 Type I diabetic patients and 6 normal subjects. All the subjects received an iv bolus injection of biosynthetic human GH, 2 IU; 2 h later they received either a. pyridostigmine, 120 mg orally, or b. placebo, 2 tablets orally, followed 1 h later by iv injection of GHRH(1-29) NH2, 100 micrograms. In normal subjects the median GH peak after GH+ GHRH was 1.8, range 1.2-6.9 micrograms/l. Pyridostigmine enhanced the GH response to GHRH in all subjects. The median GH peak after pyridostigmine + GH + GHRH was 32.7, range 19.8-42.1 micrograms/l (p less than 0.001 vs GHRH alone). Seven diabetic subjects had median GH peaks after GH + GHRH greater than 6.9 micrograms/l (the maximum GH peak after GH + GHRH in normal subjects) (group A: median GH peak 35.7, range 21.7-55 micrograms/l). The other diabetic subjects had GH peak lower than 6.9 micrograms/l (group B: median GH peak 4.4, range 2.1-6.5 micrograms/l). Pyridostigmine significantly increased the GH response to GHRH in group B patients (median GH peak 29.3, range 15.7-93.4 micrograms/l, p less than 0.001 vs GH + GHRH alone), but not in group A patients (median GH peak 39.9, range 21.9-64.9 micrograms/l). Group A diabetic patients were younger and had higher HbA1c and blood glucose levels than group B patients. In those diabetic patients with an exaggerated GH response to GH + GHRH, pyridostigmine failed to cause the increase in GH secretion observed in diabetic and control subjects with no responses to GH + GHRH.(ABSTRACT TRUNCATED AT 250 WORDS)
Heterologous radioimmunoassays for FSH and LH were employed to examine the effect of synthetic LH-RH upon gonadotrophin secretion in the ferret. Intravenous injection of 4 microng LH-RH induced a surge of FSH and of LH secretion in male and in female animals. In intact and in castrated males, the rise of LH was much more marked than that of FSH. The gonadotrophin response to LH-RH was greater in anoestrous than in oestrous females; FSH secretion was not enhanced during oestrus. Ovariectomized females behaved as anoestrous females with respect to LH secretion, while FSH secretion remained unchanged. Treatment of ovariectomized females with progesterone did not alter the pattern of response to LH-RH, but oestradiol treatment depressed the reaction to match that seen in oestrous females. Repetitive injections of LH-RH induced repetitive surges of FSH and LH in anoestrous females, but only of LH during oestrus: slow i.v. infusion of LH-RH induced a sustained elevation of plasma LH levels both in oestrous and in anoestrous females; again FSH levels rose only in anoestrous females. Injection of synthetic TRH did not alter gonadotrophin secretion in corresponding groups of male or female ferrets.
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