[Demethylchlortetracycline treatment of cirrhotic ascites with hyponatremia].
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Biomedical subjects
Publications and source records attributed to B Conte-Devolx.
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3 cases of inappropriate vasopressin secretion during one case of anaplastic carcinoma of the lung, one case of carcinoma of the prostate with bony metastases and one case of acute intermittent porphyria are presented. The plasma levels of vasopressin, measured by radioimmunoassay were high. Treatment with demeclocycline was attempted in one case. The clearance of free water was positive but the treatment was poorly tolerated by the digestive tract.
Using the radioimmunoassay (R.I.A.) for neurophysins (I.R.N.) described in 1969, we demonstrated a concomitant, rapid release of both A.D.H. and I.R.N. within the first minutes (2') of the i.v. infusion of nicotine in 11 patients with normal neuropituitary function and 1 patient suffering from a Schwartz-Bartter syndrome. There is a close relationship (r : 0,82, p less than 0.001) similar to that described by other authors, between peak levels of A.D.H. and I.R.N. in all the patients. Hence, we proved that our R.I.A. system is influenced by nicotine stimulated neurophysins (N.S.N.). The negative results previously published by two of us in 5 normal men could have been due to the length of the period between the beginning of the test and the first blood sampling (30 mn).
The authors have developed a radioimmunoassay for human plasma vasopressin (AVP) which permits the estimation of antidiuretic hormon (ADH) levels as low as 0,8 pg/ml. The average plasma level of AVP after overnight water restriction was found to be 14,3 pg/ml (sd = 4,4 pg/ml) in normal subjects. They provoked a hypersecretion of ADH by the intravenous injection of 1-2 mg of nicotine. In 11 volunteer normal subjects this stimulation by nicotine provoked ADH hypersecretion which reached a maximum between 2nd and 15th minutes after injection. In 3 cases of diabetes insipidus, nicotine injection did not induce ADH hypersecretion; in 1 case of potomania this response was weak; in 2 cases of syndrome of inappropriate ADH secretion, AVP plasma levels were elevated and the response after nicotine stimulation was exaggerated.
By means of electrical stimulation of the supraoptic nuclei, in a stereotaxic apparatus, partial or complete degranulation of the neurohypophysis is obtained, with often a continued presence of large vesicles; the number of microvesicles is always increased.
In order to elucidate the physiological role of the 41 amino-acid residue corticotropin-releasing factor (41-CRF) on the secretion of ACTH, B-Endorphin and alpha-MSH, plasma levels of these peptides were measured by radioimmunoassay in intact and adrenalectomized rats, two hours after the injection of either 41-CRF antiserum (CRF-AS) or normal rabbit serum for controls. The administration of CRF-AS strikingly lowered the plasma ACTH levels in both intact and adrenalectomized rats. A statistically significant reduction of plasma levels of B-Endorphin was also observed in the same rats. However, the effect of CRF-AS on B-Endorphin release was less pronounced than the effect on ACTH release. No changes in plasma alpha-MSH levels were observed after passive immunization with CRF-AS. We conclude that, in the rat, 41-CRF plays a physiological role in the regulation of ACTH and B-Endorphin secretion, but is not involved in the regulation of alpha-MSH release from the pituitary gland.
Passive immunization of pregnant rats with a specific antiserum to rat GRF (GRF-AS) is followed by a decrease in fetal serum GH on the 19th day of gestation. A significant reduction in serum GH is still observed in older fetuses and newborn rats. Pituitary GH content increases in 19- and 20-day-old fetuses after GRF-AS administration to their mothers. These results suggest that endogenous fetal hypothalamic GRF (or placenta GRF) play a physiological role in the secretion of pituitary GH as early as the 19th day of fetal life and may be responsible for the peak of GH release that occurs in fetuses at the end of gestation.
We have compared the release of CRF induced by potassium depolarization, noradrenaline or dopamine as monitored either during superfusion of mediobasal hypothalamus or during incubation of whole hypothalamus. The superfusion device was improved in order to prevent gas leakage and to keep constant pO2 and pCO2 in the superfusion chamber. Basal CRF secretion as well as KCl- and norepinephrine-induced CRF release were comparable in superfusion and incubation experiments. Pharmacological investigations suggest that the stimulatory effect of norepinephrine on CRF release is mediated mainly through alpha 1 and alpha 2 adrenergic receptors, and partially through beta receptors.
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A nosological entity, calloso-genital dysplasia, is described from a case of primary amenorrhoea with coloboma and total agenesis of the corpus callosum. Deficiency of the thalamic gonadotropic hormone secretion was elicited, together with normal or moderately elevated prolactinaemia, the significance of which is discussed. Thyrotropic, somatotropic and corticotropic functions were normal. It may be that the hypogonadotropic eunuchoidism of this 24-year old woman with normal olfaction evolved towards panhypopituitarism over a number of years, but in such a malformation that had not changed since birth the thalamic hypophysiotropic dysfunction seems to be fixed and stable. Unless a most unlikely coincidence occurred, the primary amenorrhoea seems to be related to the malformation. Agenesis of the corpus callosum with panhypopituitarism is well known, but this case is original in that the pituitary deficiency is very limited. A comparison with its mirror image, olfacto-genital dysplasia or Kallman's syndrome is tempting, but it remains to be documented anatomically by other cases.
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Somatostatin levels have been determined by radioimmunoassay in hypophysial portal blood of pentobarbital-anesthetized male rats. In euthyroid rats, the mean level was 158 +/- 27 pg/ml (n = 8); somatostatin was undetectable (less than 30 pg/ml) in systemic blood of these rats. Thyroidectomy and excess of T4 did not modify the levels of somatostatin in hypophysial portal blood.
Plasma DHA, DHAS and cortisol levels were measured by R.I.A. before and after intravenous and intramuscular injection of beta 1-24 ACTH. In 7 normal adult women, plasma cortisol and DHA levels rose sharply in response to beta 1-24 ACTH (0,25 mg) i. v injection; in opposition, plasma DHAS levels did not change significantly 30 and 120 minutes after the injection. In 9 normal adults women, the i. m injection of Zn beta 1-24 ACTH (1 mg) caused a significant increase in both plasma cortisol, DHA and DHAS levels 8 and 24 hours after the injection.
Immunoreactive ACTH has been found in human pituitary and plasma under different molecular forms: Big ACTH, intermediate ACTH, ACTH 1-39 and fragments of ACTH. In the literature, there are some controversies especially regarding to the importance of Big ACTH in plasma and tissue. Big ACTH is absent or present in only low amounts in plasma and pituitary extracts from normal subjects. However, the proportion of Big ACTH is very high in tumor extracts and plasma obtained from patients with ectopic ACTH syndrome High concentrations of small ACTH fragments are also present in this syndrome.
Alterations in the secretion of iodothyronines, cortisol, testosterone and growth hormone have previously been described in anorexia nervosa. We have studied prolactin and gonadotropins secretion in 23 cases of anorexia nervosa. Prolactin secretion was normal. Modifications in gonadotropins release were observed. However they could not be always related to weight loss since amenorrhea could either precede weight loss or still be present after return of the weight to normal. In all cases, FSH release after LHRH stimulation was normal. No increase in LH levels was observed after LHRH injection when the weight was 70% below the ideal weight. With increasing weight, LH release progressively recovered and normal LHRH-induced LH release was obtained when the weight was above 90% of the ideal weight. At normal weight, the ratio of LH/FSH was normal in patients menstruating less than 3 months after the test, while the ratio was low in non-menstruating females. In conclusion, when the weight was insufficient basal levels of FSH and LH and responses after LHRH stimulation corresponded to a prepuberal stage. An increase in the LH/FSH ratio and a normal LH/FSH ratio preceeded the recovery of menstruations. In about 1/3 of the cases, such an evolution was not observed without any satisfactory explanation. Other factors than weight may be involved, especially when the amenorrhea persists after weight recovery.
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