LH and FSH levels in serum and cerebrospinal fluid (CSF) of human fetus.

The concentration of LH and FSH was measured in the fetal blood and cerebrospinal fluid (CSF) of 4 human fetuses between 21 and 24 weeks old. A comparison was made with 6 post menopausal females. In one fetus the serum and CSF levels of both hormones were determined after administration of 200 micrograms LRH and 400 micrograms TRH. The mean serum fetal levels of LH and FSH of 76.6 mIU/ml (range, 29.5-152.0) and 30.5 mIU/ml (range 3.1-60.3), respectively, were not significantly different from those of postmenopausal females, whereas the fetal CSF levels of these hormones were significantly higher (p less than 0.02) than those of post menopausal females. The serum to CSF ratios for the fetal LH and FSH were 4.6 +/- 1.1 and 2.4 +/- 0.61 respectively, significantly different (p less than 0.02 and p less than 0.001 respectively) from those of post menopausal females (29.1 +/- 6.6 for LH and 50.9 +/- 10.9 for FSH). In one fetus LRH did not provoke any change in circulating FSH and LH level 20 min. after administration, while a slight increase of these hormone in the CSF was observed. These data suggest that the permeability of blood-CSF barrier to gonadotropins in the fetus seems to be higher than in the adult who has no blood-CSF barrier (B--CSF--B) alterations.

LH and FSH in human cerebrospinal fluid.

LH and FSH of cerebrospinal fluid (CSF) and serum were radioimmunologically measured. Samples were obtained simultaneously from 116 subjects of the following groups: A. 22 patients with non-endocrine diseases, B. 18 patients with cranial diabetes insipidus (DI) of whom 4 with metastatic carcinomas, C. 5 patients with primary empty sella syndrome, D. one with hydatiform mole, and E. 70 patients with pituitary adenomas, i.e. growth hormone--or prolactin-secreting or "non-secreting" adenomas, of whom 38 patients with invasive and 32 with enclosed adenomas. LH and FSH are normal constituents of CSF and their CSF levels poorly correlates with the serum ones (LH r = 0.477 p less than 0.01). Enclosed adenomas with SSE showed low levels of LH in CSF. High CSF-gonadotropins concentrations (above 4.0 mIU/ml) with a low serum/CSF ratio (below 3) was frequently, but not constantly found in patients with invasive adenomas and are not indicative per se of this diagnosis. Some patients with brain metastasis from breast carcinoma and DI, or with non-tumoral diseases and DI showed similar high patterns of CSF gonadotropins though the serum levels were within normal range. This suggests that local vascular mechanisms, including the retrograde circulation of gonadotropins from the pituitary to the hypothalamus, influence the blood-brain barrier much more than the release of gonadotropins into the systemic blood circulation.

Mixed TSH- and HGH-secreting pituitary adenoma.

A man aged 36 was found to have an invasive pituitary adenoma with evolutive acromegaly and hyperthyroidism and a high serum level of HGH and TSH, suggesting a tumoral production of HGH and TSH. The serum concentration of HGH was above 180 ng/ml; there was also an inappropriately high serum level of TSH, which failed to decrease following the triiodothyronine suppression test and did not increase after TRH (0.4 mg i.v.). In the tumoral tissue removed during pituitary surgery, the concentration of TSH was 1,267.2 microU/g and that of HGH was 1,158.6 micrograms/g, showing that the pituitary adenoma secreted both TSH and HGH.

Blood-cerebrospinal fluid barrier for prolactin in empty sella syndrome.

In six patients with "empty sella" syndrome (ESS), three primary (pESS) and three secndary (sESS), the ratio of serum to cerebrospinal fluid (CSF) concentrations of prolactin (PRL) was 6.6 +/- 0.7 (mean +/- SEM) (range 5.5--9.6), with a significant correlation between serum and CSF levels of PRL (r = 0.93 p less than 0.01). A control group of ten normal subjects showed similar values. The hyperprolactinemia found in two cases of pESS did not change the serum/ CSF ratio of PRL. The acute release of PRL into the serum following TRH i.v. did not increase the PRL level in CSF either in control subjects or ESS, with one exception. In a case of sESS consecutive to the treatment with bromocriptine (for 6 months) of an invasive prolactinoma, TRH i. v. released PRL into the CSF but not into the blood, and the serum/ CSF ratio of PRL was very low, until a new cure with bromocriptine (for 3 months) mormalised it. It is suggested that the blood-CSF barrier for PRL is similar in ESS and in normal subjects, with the exception of sESS following incomplete remission of some invasive prolactinomas, in which the high permeability of BCB may be explained both by hemodynamic changes in the pituitary portal vascular system and by a new source of PRL which release it directly into the CSF, bypassing the blood route.

Influence of arginine vasotocin administration on nocturnal sleep of human subjects.

Arginine vasotocin (AVT) or placebo were subcutaneously administered to 4 men at 22.00 and 01.00 h, along four nights, and polygraphic recordings were performed between 22.00 and 02.00 h during sleep. AVT significantly increased only the amount of rapid eye movement (REM) sleep (p less than 0.05), but did not influence the latency of the first REM sleep period. This effect of AVT was not dose dependent in the range between 2 and 12 microgram AVT. AVT or placebo were also intravenously injected or perfused to 10 normal adult subjects, at different times of the day, under clinical control. Doses between 2 microgram perfused 4 h and 12 microgram perfused 30 min, did not produce clinical signs of sleep. It is suggested that AVT is not a blood factor for inducing of slow waves sleep (SWS) or REM sleep in humans.