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L Martini

Publications and source records attributed to L Martini.

At least 163 records · Page 9Linked to original sources
PubMed1987

In vitro release of luteinizing hormone-releasing hormone from the hypothalamus of old male rats.

The present experiments tested the ability of the hypothalamus of old male rats to release LHRH in vitro. Mediobasal hypothalami (MBH) of 18-month-old and 6-month-old male rats were perfused for a total of 5 h and 5 min; the amounts of LHRH released, both in basal conditions and after stimulation with high extracellular K+ (110 mM, applied for 5 min every 30 min), were measured in the effluent. Our results show that the basal secretion of LHRH from the perfused MBH of young and old male rats is quantitatively similar. Moreover, the MBHs of young and old animals are capable of responding to the repeated administration of a K+ stimulus with repeated bursts of LHRH hypersecretion. From a quantitative point of view, the MBHs of old animals respond to the K+ stimulus in a fashion similar to that found in younger animals; even if the responses to K+ of the hypothalami of old animals appear to be somewhat lower than those of the hypothalami of younger animals, the differences recorded were not significant. LHRH content (as measured by RIA) of the MBH before the perfusion period was similar in young and old animals. At the end of the experiment, the content of LHRH of the perfused hypothalamus was not significantly different in the old and young groups. Serum and intrapituitary levels of LH and FSH were significantly lower in 18-month than in 6-month-old animals. These data suggest that the alterations of the function of the hypothalamic-pituitary-gonadal complex observed in aged male rats are not due to an intrinsic age-related defect of LHRH-synthesizing neurons.

Aging↗
PubMed1987

Ultrashort feedback control of luteinizing hormone-releasing hormone secretion in vitro.

The present experiments were performed to clarify whether LHRH might inhibit its own secretion via an ultrashort feedback mechanism acting directly on the hypothalamus. Using an in vitro system, mediobasal hypothalami (MBHs) of adult male rats were perifused in either the presence or absence of a LHRH agonistic analog [D-Ser(TBU)6,Des-Gly10] LHRH ethylamide shown not to cross-react in the LHRH RIA. In the first series of experiments, six MBHs per chamber were initially perifused with control medium and submitted to two K+ stimulations (110 mM) for 5 min every 30 min; the control medium was then replaced by medium containing the LHRH analog (5 microM), and three additional K+ pulses were applied. In the second series of experiments, a single MBH per chamber was exposed for the duration of the experiments to either control medium or medium containing the LHRH analog (5 microM). In both cases, pulses of K+ were applied to the tissue. The amounts of endogenous LHRH released both under basal conditions and after K+ stimulation were measured in the effluent (1 ml every 5 min) with a specific RIA. The results show that the LHRH analog inhibits basal secretion of endogenous LHRH from the MBH, and diminishes or abolishes the response to K+ stimulations. The specificity of the inhibitory effect exerted by the LHRH analog on LHRH secretion was shown by the inability of TRH to mimic the effect of the LHRH analog. The data are consistent with the hypothesis that LHRH, acting at a hypothalamic level, might participate in the control of its own release via an ultrashort feedback mechanism.

Animals↗
PubMed1987

Further evidence that gonadal steroids do not modulate brain opiate receptors in male rats.

It is still unclear whether, in the male rat, castration and androgen replacement affect the binding characteristics of brain opiate receptors. To clarify this issue, the effects exerted by orchidectomy and testosterone (T) replacement on the subpopulation of brain mu opiate receptors were studied in male rats; testosterone was administered via subcutaneous Silastic capsules. Utilizing 3H-dihydromorphine (a mu receptor ligand) it has been shown that the affinity constant (Ka) of brain mu opiate binding sites, measured in plasma membrane preparations, is not affected by castration. When mu receptor concentrations were measured in individual brains, it was found that gonadectomy and T replacement failed to produce any change in the number of mu opiate receptors. These data suggest that, in male rats, gonadal steroids do not develop their central feedback effects by affecting brain mu opiate receptors.

Animals↗
PubMed1987

[Human leptospirosis in New Caledonia and dependencies. Apropos of 57 cases observed between 1 June 1983 and 31 May 1985].

57 cases of leptospirosis were diagnosed in New Caledonia (South Pacific French Territory) between June 1983 and May 1985. 25% cases are severe infections; thrombopenia and renal failure are frequently observed. Leptospires are found in blood or spinal or urine culture confirmed by haemagglutination tests on microplates (Martin et Petit). Epidemiological studies are being performed during 1985-1986 to devise preventive measures adapted to the territory.

Adult↗
PubMed1987

Circatrigintan rectal temperature and endocrine rhythms of clinically healthy, menstrually cycling women.

Rectal temperatures were measured automatically every 10 min for part or most of two menstrual cycles in ten clinically healthy young women, 20-30 years of age, with a wearable instrument, the Polychronor. Occasional malfunction of the instrumentation resulted in corresponding gaps in the series. Data were examined by chronograms, plexograms, and chronobiologic serial sections computed with the fit of a 24-hr period, population-mean cosinor, and linear-nonlinear least-squares analyses. Single cosinor-derived circadian parameters were next fitted with a cosine curve of a period equal to the number of days of the corresponding intermenstruum. Second-order infradian inferential statistics were calculated next; the first day of menstruation was used as acrophase reference. A population-mean cosinor at the intermenstrual period yields a temperature acrophase of -279 degrees, with the 95% confidence interval extending from -254 degrees to -312 degrees. Since the intermenstruum differs in different subjects and/or in different menstrual cycles of a given woman, this acrophase corresponds to different time intervals from the first day of menstruation in different cases. This acrophase thus indicates the relative timing within the menstrual cycle of overall high rectal temperatures. On four subjects in four stages of their menstrual cycle, plasma was also obtained at 2-hr intervals around the clock. Ten hormones were determined. The sparse endocrine sampling along the menstrual cycle notwithstanding, a circatrigintan rhythm in all hormones investigated was demonstrated for a woman 26 years of age. At the period corresponding to the intermenstrual interval, the acrophases for T3, cortisol, FSH, testosterone, DHEA-S, T4, and LH occurred before the circatrigintan rectal temperature acrophase, whereas the acrophases for prolactin, estradiol, and progesterone occurred near or shortly after the rectal temperature acrophase. Whereas earlier circatrigintan mapping of adult women had been summarized on a group basis, this study allows individualized circatrigintan rhythm assessment. Circatrigintan, like circadian and circannual, acrophase and amplitude relations do not necessarily imply causal relations, yet they are an indispensable quantitative reference standard for the study of basic mechanisms and for diagnosis and intervention, including endeavors in planned parenthood that might take into account the organism's dynamics with multiple frequencies.

Adult↗
PubMed1986

Studies on the possible existence of two 5 alpha-reductases in the rat prostate.

In the first group of experiments, the in vitro metabolism of labelled testosterone has been studied in the ventral prostate of young (2 months) and old (15 and 22 months) male rats. It has been found that the prostate of 2-month-old animals converts testosterone into dihydrotestosterone (5 alpha-androstane-17 beta-ol-3 one, DHT) and into the diols (5 alpha-androstane-3 alpha-17 beta-diol and 5 alpha-androstane-3 beta,17 beta-diol) with considerable yields. The prostate of young animals is also able to convert testosterone into delta 4-androstenedione (delta 4-A), 5 alpha-androstanedione (5 alpha-A) and androsterone (A); however, the amounts of these metabolites are lower than those of DHT and the diols. It has been found that ageing induces major alterations in the prostatic metabolism of testosterone. In particular, a progressive and significant decrease in the formation of DHT and of the diols has been found in animals of 15 and 22 months of age. Advancing age induces, on the contrary, an increase of the formation of delta 4-A and of the 5 alpha-reduced metabolites of the 17-keto series (5 alpha-A + A). In the second group of experiments, the effects exerted by 4-hydroxy-4-androstene-3,17-dione (4-OH-A) on the in vitro metabolism of labelled testosterone and delta 4-A in the ventral prostate of adult male rats have been studied. It has been found that 4-OH-A, when added to the incubation media, decreases the formation of DHT and of the diols, when labelled testosterone is used as the substrate. The presence in the media of this steroid enhances the formation of delta 4-A and of 5 alpha-A. The transformation of labelled delta 4-A into 5 alpha-A is not modified by the presence in the medium of 4-OH-A. From the two groups of experiments, it is concluded that in the ventral prostate of the rat there are two different 5 alpha-reductase isoenzymes, one sensitive to age and to the inhibitory effect of 4-OH-A (and which is responsible for the conversion of testosterone into the 5 alpha-reduced metabolites of the 17-OH series, DHT and the diols), and a second one, insensitive to age and to the effects of 4-OH-A, which affects the conversion of delta 4-A into 5 alpha-A.

3-Oxo-5-alpha-Steroid 4-Dehydrogenase↗
PubMed1986

In vitro metabolism of testosterone in the rat prostate: influence of aging.

The in vitro metabolism of labelled testosterone has been studied in the ventral prostate of young (2 months) and old (15 and 22 months) male rats. It has been found that the prostate of 2-month old animals converts testosterone into dihydrotestosterone (5-alpha-androstane-17-beta-ol-3-one, DHT) and into the diols (5-alpha-androstane-3-alpha,-17-beta-diol and 5-alpha-androstane-3-beta,17-beta-diol) with considerable yields. The prostate of young animals is also able to convert testosterone into delta-4-androstenedione (delta-4-A), 5-alpha-androstanedione (5-alpha-A) and androsterone (A); however, the amount of these metabolites are lower than those of DHT and the diols. Aging induces major alterations in the prostatic metabolism of testosterone. In particular, a progressive and significant decrease in the formation of DHT and of the diols has been found in animals of 15 and 22 months of age. Advancing age induces, on the contrary, a progressive and significant increase of the formation of delta-4-A. The total amounts of 5-alpha-reduced metabolites of the 17-keto series (5-alpha-A + A) are higher at 15 and 22 months than at 2 months of age. This increase appears to result from an enhanced formation of 5-alpha-A at 15 months, and of A at 22 months. The present data show that aging exerts important effects on the metabolism of testosterone in the ventral prostate of the rat. The results may help explaining why the old rat does not develop spontaneously the syndrome of benign prostatic hypertrophy (BPH), as it occurs in other species (dogs and humans).

Aging↗
PubMed1986

Effect of 1,4,6-androstatriene-3,17-dione (ATD), 4-hydroxy-4-androstene-3,17-dione (4-OH-A) and 4-acetoxy-4-androstene-3,17-dione (4-Ac-A) on the 5 alpha-reduction of androgens in the rat prostate.

The present study reports the effects exerted by 1,4,6-androstatriene-3,17-dione (ATD), 4-hydroxy-4-androstene-3,17-dione (4-OH-A) and 4-acetoxy-4-androstene-3,17-dione (4-Ac-A), three steroids known to inhibit the aromatization of androgens to estrogens, on the in vitro metabolism of labelled testosterone (T), dihydrotestosterone (DHT) and androstenedione (delta-4-A) in the ventral prostate of adult male rats. It has been found that ATD, in the concentration tested, does not influence the conversion of labelled T into DHT, but decreases the formation of 5 alpha-androstane-3 alpha,17 beta-diol and 5 alpha-androstane-3 beta,17 beta-diol (diols). On the contrary, 4-OH-A and 4-Ac-A simultaneously decrease the formation of DHT and the diols. When T is used as the substrate, the presence in the medium of these three steroids enhances the formation of delta-4-A and of 5 alpha-androstanedione (5 alpha-A). ATD, but not 4-OH-A and 4-Ac-A inhibits the conversion of labelled DHT into the diols. The transformation of labelled delta-4-A into 5 alpha-A is not modified by either ATD or 4-OH-A, while 4-Ac-A exerts only a small inhibition. These results suggest that the three aromatase inhibitors tested are able to profoundly modify the metabolism of T in the ventral prostate of the rat. In particular: 4-OH-A and 4-Ac-A are able to inhibit the conversion of T into DHT; ATD is able to inhibit the conversion of DHT into the diols; ATD and 4-OH-A do not inhibit the process of 5 alpha-reduction of delta-4-A into 5 alpha-A, while 4-Ac-A exerts only a minor effect. It is suggested that in the ventral prostate of the rat there are two different 5 alpha-reductase isoenzymes, one sensitive to the inhibitory effect of the steroid tested and which is responsible for the conversion of T into the 5 alpha-reduced metabolites of the 17-OH series (DHT and the diols), and a second one, insensitive to the effects of the three steroids, which affects the conversion of delta-4-A into 5 alpha-A.

Androgens↗
PubMed1986

Stimulatory and inhibitory effects of the opioids on gonadotropin secretion.

In order to gain additional information on the role played by the opioids in the control of the secretion of anterior pituitary gonadotropins, morphine (an opioid agonist) and naloxone (an opioid antagonist) have been injected intraventricularly (i.v.t.) into normal or castrated male rats. The animals were killed by decapitation at different time intervals after treatment and serum luteinizing hormone (LH), follicle-stimulating hormone (FSH) and prolactin were measured by radioimmunoassay. Animals injected i.v.t. with 0.9% saline solution and sacrificed at the same time intervals served as controls. When morphine (at the dose of 200 and 400 micrograms/rat) and naloxone (at the dose of 7.5 and 15 micrograms/rat) were injected i.v.t. into normal male rats, a significant increase of serum levels of LH was observed 10 and 20 min after injection. There was no effect at 5, 40 and 60 min. Lower doses of morphine (6.25, 12.5, 25, 50 and 100 micrograms/rat) given i.v.t. were ineffective. When morphine (200 micrograms/rat) and naloxone (either in the dose of 7.5 micrograms/rat or of 15 micrograms/rat) were given simultaneously, serum LH was significantly higher than in the saline-treated controls both at 10 and 20 min. However, the increases of serum LH levels induced by the combined treatment were in both instances lower than those produced by the administration of either drug alone. Morphine (200 micrograms/rat) when administered i.v.t. to normal male rats significantly enhanced prolactin release at 10 and 20 min, and this effect of morphine was blunted by the concomitant i.v.t. administration of naloxone (7.5 and 15 micrograms/rat).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1986

In vitro effects of an aromatase inhibitor on 5 alpha-reductase activity in human hypertrophic prostatic tissue.

To determine the effects of 4-hydroxy-4-androstene-3,17-dione (4-OH-A) on the in vitro conversion of testosterone (T) to 5 alpha-androstan-17 beta-ol-3-one (dihydrotestosterone, DHT), 5 alpha-androstan-3 alpha, 17 beta-diol and 5 alpha-androstan-3 beta, 17 beta-diol (diols), human benign hypertrophic prostatic (BPH) tissue was incubated with 4-14C-T as substrate, in the presence of 4-OH-A (10(-8) to 10(-6) M); the amounts of the 5 alpha-reduced metabolites formed were quantitated. The effects of 4-OH-A were compared with those of 17 beta-N,N-diethylcarbamoyl-4-methyl-4-aza-5 alpha-androstan-3-one (4-MA), a known inhibitor of the 5 alpha-reductase. In the absence of 4-OH-A and 4-MA, human BPH tissue converted T to DHT and the diols readily. Both 4-OH-A and 4-MA induced significant and dose-related decreases in the formation of both DHT and the diols. The degree of inhibition induced by the different concentrations of 4-OH-A and 4-MA were 31, 41, 72% and 57, 87, 97%, respectively. The decreased formation of the diols was a consequence of the decreased availability of DHT (the immediate precursor of the diols) and was not due to direct effects of the inhibitors on the 3-hydroxysteroid dehydrogenases; both 4-OH-A and 4-MA were totally unable to modify the conversion of DHT to the diols, when 4-14C-DHT was used as substrate. Thus, 4-OH-A inhibits the process of 5 alpha-reduction of T in BPH tissue. This molecule might represent a potential new agent for the prevention and/or treatment of human BPH.

5-alpha Reductase Inhibitors↗
PubMed1986

Morphine stimulates prolactin release in normal but not in castrated male rats.

Morphine (200 micrograms/rat) was injected intraventricularly (i.v.t.) into normal and into long-term castrated (4 weeks) adult male rats. Animals were killed 10, 20, 40 and 60 min after treatment. In normal animals, the treatment with morphine resulted in a significant increase of serum prolactin concentrations at all time intervals considered. However, the i.v.t. injection of 200 micrograms morphine/rat into castrated rats did not exert any significant effect on prolactin release at any time interval considered. When morphine (200 micrograms/rat) was administered i.v.t. together with the specific opioid receptor blocker naloxone (7.5 or 15 micrograms/rat) the stimulatory effect of morphine on prolactin release was diminished at 10 min, and totally blocked at 20 min. Naloxone given alone did not influence serum prolactin concentrations. The results suggest that the presence of endogenous androgens is essential to permit the stimulatory effect of morphine on prolactin release.

Animals↗
PubMed1986

[Neurologic manifestations of ciguatera. 3 cases with a neurophysiologic study and examination of one nerve biopsy].

Ciguatera is the commonest form of poisoning resulting from eating fish in the tropics. It has been recognised since the 15th century. The disease is due to the formation of ciguatoxin by a dinoflagellate, Gambierdiscus toxicus, loosely attached to algae growing on coral reefs. The toxin, which is harmless to the fish, is ingested by small herbivorous fish and passes up the food chain as these are eaten by carnivores. The toxic effects include gastroenteritis, itching of the skin, peripheral neuropathy and central nervous system dysfunction. Though most cases are mild, occasionally the disease is severe and even fatal. There is no effective specific treatment. Three cases, of which one died and which exhibited both peripheral and central nervous system involvement, are described. Histological changes in sural nerve fibers are described. There was striking oedema of the adaxonal Schwann cell cytoplasm. These histological changes are very similar to those seen following the injection of scorpion and spider venoms into the peripheral nerve of experimental animals. Both these venoms and ciguatoxin increase the permeability of the membrane to sodium.

Adult↗
PubMed1985

Effect of naloxone on luteinizing hormone, follicle-stimulating hormone, and prolactin secretion in the different phases of the estrous cycle.

It is becoming increasingly clear that the effects exerted by opioid agonists and antagonists on the release of gonadotropins and of PRL may vary according to the endocrine milieu. To investigate this issue further, female rats with a regular 4-day estrous cycle have been injected sc with the opioid antagonist naloxone at different hours of the day, during each of the various days of the estrous cycle. The animals were killed 20 min after the sc administration of naloxone (2.5 mg/kg dissolved in 0.9% saline solution) at 1000 and 1600 h on the first and second day of diestrus and at 1000, 1200, 1400, 1600, 1800, and 2000 h on proestrus and estrus. Animals were killed by decapitation, and trunk blood was collected and assayed for LH, FSH, and PRL. The data obtained from naloxone-treated animals were compared to those derived from controls injected sc with 0.9% saline solution and killed at the same time intervals. The sc injections of naloxone stimulated LH release in every phase of the estrous cycle; however the magnitude of the responses was highly variable. Increases of the order of 700-1.000% were observed during the 2 days of diestrus, at 1000 and 1400 h of the day of proestrus, and at 1600, 1800, and 2000 h of the day of estrus. Much higher responses (of the order of 2.700-3.300%) were observed at 1600 h of the day of proestrus and at 1000, 1200, and 1400 h of the day of estrus. The LH response to naloxone appeared to be obliterated at 1800 and 2000 h of the day of proestrus. Serum levels of FSH and PRL were not affected by the treatment at any of the time intervals considered. These findings suggest that, in normally cycling adult female rats, naloxone exerts a stimulatory effect on LH release during each day of the estrous cycle; that the stimulatory effect of naloxone is minimal at the time of the spontaneous proestrous LH surge; and that the effect of naloxone on LH release is, on the contrary, maximal just before the spontaneous proestrous LH surge and up to 1400 h of the day of estrus. The observation that naloxone does not affect FSH and PRL release underlines once more that the central mechanisms controlling LH, FSH, and PRL secretion are different.

Animals↗
PubMed1985

Induction of precocious puberty in the female rat after chronic naloxone administration during the neonatal period: the opiate 'brake' on prepubertal gonadotrophin secretion.

Studies were undertaken using the opiate receptor antagonist naloxone to examine the hypothesis that endogenous opiates may have a restraining effect on prepubertal gonadotrophin secretion and may be involved in the maturation of the central nervous system mechanisms regulating the onset of puberty in the female rat. Naloxone (2.5 mg/kg) administered intraperitoneally every 6 h to female rats from day 1 to day 10 of postnatal life significantly (P less than 0.001) advanced the age of onset of puberty assessed in terms of the day of vaginal opening and first oestrus (32.3 +/- 0.2 vs 40.8 +/- 0.4 days in control saline-treated animals). Animals so treated with naloxone showed significantly (P less than 0.001) higher levels of FSH (761.4 +/- 87.6 vs 483.8 +/- 57.2 micrograms/l in control animals) and LH (562.8 +/- 57.4 vs 351.3 +/- 43.3 micrograms/l in control animals) at the first late pro-oestrus and a significantly (P less than 0.001) higher number of ova released at first oestrus (12.4 +/- 0.4 vs 8.1 +/- 0.3 in controls). Body weight at first oestrus was significantly (P less than 0.001) lower in the naloxone-treated animals, an indication that these animals were much younger. The weights (per 100 g body wt) of the ovaries and uteri at the first oestrus were significantly (P less than 0.01) higher in the naloxone-treated rats than in the controls. However, there were no significant differences in the weights of the adrenals and anterior pituitary glands between the two groups of animals.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1984

Effects of bromocriptine and naloxone on plasma levels of prolactin, LH and FSH during suckling in the female rat: responses to gonadotrophin releasing hormone.

The roles of dopamine and the endogenous opiate peptides in the mediation of the inverse relationship between prolactin and gonadotrophin secretion during lactation were studied by comparing the effects of bromocriptine and naloxone on plasma levels of prolactin, LH and FSH during suckling in the female rat. The effects of exogenous gonadotrophin releasing hormone (GnRH) on the LH and FSH responses to bromocriptine and naloxone were also assessed. In control animals (saline), there was a marked fall in LH levels and a large increase in prolactin levels within 15 min of suckling. In response to GnRH (25 ng) there was a small progressive increase in LH levels reaching a maximum at 45 min. Both bromocriptine (500 micrograms) and naloxone (500 micrograms) markedly suppressed the suckling-induced prolactin surge when administered in two separate groups of animals. However, despite the bromocriptine-induced suppression of prolactin levels, there was no increase in LH levels which remained low throughout the suckling period. Naloxone (500 micrograms), however, induced a twofold increase in LH levels within 15 min suggesting that an enhanced opiate rather than dopaminergic activity may be responsible for the suppression of GnRH and hence gonadotrophin secretion during suckling. This is supported by the finding that whereas combined bromocriptine (500 micrograms) and GnRH (25 ng) treatment suppressed the suckling-induced prolactin rise and also induced only a small progressive increase in LH (similar to GnRH alone), combined naloxone (500 micrograms) and GnRH (25 ng) treatment induced a sharp sixfold increase in LH levels within 15 min while at the same time markedly suppressing prolactin levels. None of these drug treatments affected the levels of FSH.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗