摘要:

The 14CO2 production from glucose U-14C was studiedin hypothalamus and cerebral cortex of the following groups of rats: normal males, normale females during the different phases of the sexual cycle, androgenized females, and castrated females. 14CO2 production was significantly higher in the hypothalamus during estrus than in diestrus. Males and androgenized females showed values similar to those found in diestrous rats. The oxidative activity in the hypothalamus of 7-day castrated rats is similar to that observed in diestrous rats and lower than the activity found during estrous and in 30-days castrated rats. Between the different groups studied, no modifications were found in the respiratory activity of the cerebral cortex.

ISSN:0028-3835    

DOI:10.1159/000122144

出版商:S. Karger AG    

年代:1973

数据来源: Karger

摘要:

Synthetic LRH was injected i.v. innormal menstruating women and in patients with various endocrine disorders, such as retarded growth, precocious onset of puberty, anovulation, secondary amenorrhea, Sheehan’s syndrome, menopause, cryptorchidism, and Klinefelter’s syndrome. A linear log dose response relationship for LH release was found after injection of 12.5, 25, and 50 µg and, for FSH release, following injection of 6, 12, and 24 µg LRH. Maximal LH responses to a given test dose of 25 µg LRH in eu- and amenorrheal women differed significantly (p < 0.05). No difference in LH peak occurrence time was noted between the two groups. In 8 out of 120 individuals, no LH release was detected, e.g., in Sheehan’s syndrome and in retarded growth. In hypogonadal and hypergonadotropic subjects, an overresponsiveness of the pituitary to LRH stimuli was noted. Overresponsiveness was also observed in a peripubertal girl. The data presented support the concept of the pituitary sensitivity to exogenous LRH depending on the degree of endogenous gonadotropin releasing hormone sti

ISSN:0028-3835    

DOI:10.1159/000122145

出版商:S. Karger AG    

年代:1973

数据来源: Karger

摘要:

The data reported provide evidenceto support the concept of a neural regulation of growth hormone (GH) secretion in mammals. Electrolytic lesions in discrete hypothalamic areas result in a reduction of pituitary and plasma radioimmunoassayable (RIA) GH levels and stunting of growth in animals, or impair the acute GH re-sponse to the stimulus of insulin hypoglycemia. Conversely, increases in plasma GH are present after electrical stimulation of brain areas. Hypothalamic regulation of GH secretion would seem to be exerted through a neurohormone designated GH-releasing hormone (GH-RH), which has been characterized by a bioassay system. GH-RH has been purified, isolated, and synthesized and appears to be a straight-chain acidic decapeptide; however, the lack of effect of GH-RH on the release of RIA-GH, either in vitro or in vivo, introduces some elements of uncertainty and the problem is further compounded by contradictions between bioassay and RIA data in the rat. Proof has recently been afforded for the existence of an inhibitory hypothalamic factor (GIF), the physiological significance of which in the control of GH secretion remains to be established. GH-RH decreases in the hypothalamus and increases in the plasma in situations where GH release is enhanced, thus stressing the importance of the neurohormonal mechanism. Pharmacological studies in animals and in humans support the concept that the adrenergic system plays a significant role in the neurohormonal control of GH secretion. Serum GH is acutely increased in humans, following ingestion of L-dopa, an aminoacid precursor of dopamine; conversely, chlorpromazine, an antiadrenergic drug, is effective in depressing GH levels. A pattern of intermittent bursts of GH secretion is present in humans during the time of deeper sleep, apparently independent of alterations in brain catecholamine turnover. Finally, like other anterior pituitary hormones, GH appears to feed back on itself to decrease its own secretion.

ISSN:0028-3835    

DOI:10.1159/000122146

出版商:S. Karger AG    

年代:1973

数据来源: Karger

摘要:

A single injection of 0.5 µU synthetic arginine vasotocin (AVT) into the third cerebral ventricle of the mouse on the day of surgery completely inhibited the compensatory ovarian hypertrophy (COH) measured 8 days later. The same dose of AVT injected intravenously was ineffective, strongly suggesting that AVT acts centrally to inhibit COH

ISSN:0028-3835    

DOI:10.1159/000122147

出版商:S. Karger AG    

年代:1973

数据来源: Karger

ISSN:0028-3835    

DOI:10.1159/000122148

出版商:S. Karger AG    

年代:1973

数据来源: Karger

ISSN:0028-3835    

DOI:10.1159/000122149

出版商:S. Karger AG    

年代:1973

数据来源: Karger

ISSN:0028-3835    

DOI:10.1159/000122143

出版商:S. Karger AG    

年代:1973

数据来源: Karger