Biomedical subjects

A M Ossino

Publications and source records attributed to A M Ossino.

9 recordsLinked to original sources

PubMed1998

Activin-A stimulates hypothalamic gonadotropin-releasing hormone release by the explanted male rat hypothalamus: interaction with inhibin and androgens.

The presence of activins in those hypothalamic regions containing gonadotropin-releasing hormone (GnRH)-secreting neurons suggests that these peptides may regulate the reproductive function modulating not only pituitary FSH release and biosynthesis, but also hypothalamic GnRH release. The purpose of this study was to evaluate the effects of activin-A, a homodimer of inhibin beta A subunit, on hypothalamic GnRH release in vitro and, because of their well known antithetical effects, to evaluate its interaction with inhibin. In addition, since androgens modulate the release of GnRH from male rat hypothalami, we thought it of interest to study the possible interplay between these steroids and activin on GnRH release. To accomplish this, we employed a hypothalamic organ culture system which enabled us to evaluate GnRH release from individually incubated hemi-hypothalami explanted from male rats. Activin-A stimulated GnRH release in a biphasic manner. The maximal effect was reached at a concentration of 10 ng/ml which increased GnRH output by about 75%. Inhibin abolished the stimulatory effect of a maximally effective concentration of activin-A in a dose-dependent manner, whereas alone it had no effect on GnRH output. As previously shown, testosterone (1 nmol/l) and dihydrotestosterone (DHT, 0.1 nmol/l) suppressed basal GnRH release, but only testosterone was able to inhibit the release of GnRH stimulated by activin-A. Since DHT is a non-aromatizable androgen, we evaluated whether the inhibitory effect of testosterone was due to its in vitro conversion into 17 beta-estradiol. The addition of 4-hydroxyandrostenedione, a steroidal aromatase inhibitor, did not influence the suppressive effect of testosterone on GnRH release stimulated by activin-A. In conclusion, activin-A stimulated hypothalamic GnRH release in vitro and this effect was abolished by inhibin and was blunted by testosterone. These findings suggest that activins may participate in the regulation of the hypothalamic-pituitary-gonadal axis by modulating GnRH release. The ability of testosterone to suppress the release of GnRH stimulated by activin-A indicates that this steroid has a potent negative feedback influence on GnRH release.

Activins↗

PubMed1998

Endothelin (ET)-1 and ET-3 inhibit estrogen and cAMP production by rat granulosa cells in vitro.

Endothelin (ET)-1 and ET-3, two peptides with a potent vasoconstrictive property, produce a variety of biological effects in different tissues by acting through two different receptors, the ET-1 selective ET(A) receptor and the non-selective ETB receptor. An increasing body of literature suggests that ET-1 acts as a paracrine/autocrine regulator of ovarian function. Indeed, ETB receptors have been identified in rat granulosa cells and ET-1 is a potent inhibitor of progesterone production. In contrast, inconsistent data have been reported about the role of ET-1 on estrogen production and the effects of ET-3 are not known. Therefore, the present study was undertaken to evaluate the effects of ET-1 and ET-3 on estrogen and cAMP production, and the receptor type involved. Given that prostanoids modulate ovarian steroidogenesis and that many actions of ETs are mediated by these compounds, we also evaluated whether the effects of ETs on estrogen and cAMP production might be prostanoid-mediated. ET-1, ET-3, and safarotoxin-S6c (SFX-S6c), a selective ETB receptor agonist, inhibited basal estrogen production by granulosa cells obtained from immature, estrogen-primed female rats, in a concentration-dependent manner. All three peptides were also capable of inhibiting the production of estrogen stimulated by a half-maximal (1 mIU/ml) and a maximally stimulatory (3 mIU/ml) concentration of FSH, ET-1 and ET-3 dose-dependently suppressed basal and FSH (1 mIU/ml)-stimulated cAMP production. ET-3 and SFX-S6c were significantly more potent than ET-1 in suppressing estrogen production, suggesting that this effect was not mediated by the ET(A) receptor. Indeed, BQ-123, a selective ET(A) receptor antagonist, did not influence the inhibitory effects of ET-1 and ET-3 on basal and FSH-stimulated estrogen release. To determine a possible involvement of prostanoids, we evaluated the effects of maximally effective concentrations of ET-1 and ET-3 on estrogen and cAMP production in the presence of indomethacin, a prostanoid synthesis inhibitor. This compound did not have any effect on the suppressive effects of ETs on basal or FSH (1 mIU/ml)-stimulated estrogen or cAMP production. In conclusion, ET-1 and ET-3 were able to inhibit estrogen and cAMP production by rat granulosa cells, indicating that the inhibitory effects of ETs on ovarian steroidogenesis are not limited to progesterone biosynthesis. This effect does not appear to be mediated by prostanoids or by the classical ET(A) and ETB receptors, at least under these experimental conditions.

Animals↗

PubMed1996

Interaction between prolactin and catecholamines on hypothalamic GnRH release in vitro.

Brain catecholamines have been implicated in the regulation of gonadotrophin release. It has been recently reported that noradrenaline (NA), applied within the hypothalamic paraventricular nucleus, suppresses the pulsatile release of LH in the rat through a corticotrophin-releasing hormone (CRH)-dependent mechanism. Prolactin (PRL) is also able to suppress hypothalamic GnRH release following activation of the CRH-releasing neurone. Given that PRL stimulates the release of NA from hypothalamic explants and that NA stimulates the release of hypothalamic CRH, we hypothesized that this neurotransmitter may be involved in the intrahypothalamic neuroendocrine circuit mediating the inhibitory effects of PRL on GnRH release. To test this hypothesis, we evaluated the effects of PRL on GnRH release in the presence of alpha- or beta-adrenergic receptor antagonists using a static hypothalamic organ culture system which enabled us to evaluate immunoreactive GnRH (iGnRH) release from individually incubated, longitudinally halved hypothalami. As previously shown, PRL at a concentration of 100 nM inhibited basal iGnRH release by about 35%. Phentolamine, a non-selective alpha-adrenergic receptor antagonist, prazosin, an alpha 1-receptor antagonist, and yohimbine, an alpha 2-receptor antagonist, overcame the inhibitory effect of PRL on iGnRH release in a concentration-dependent fashion. In contrast, propranolol, a non-selective beta-adrenergic receptor antagonist, atenolol, a beta 1-receptor antagonist, and ICI-118,551, a beta 2-receptor antagonist, had no effect. None of these compounds had any effect on basal iGnRH release. These findings suggested that an alpha-adrenergic mechanism is involved in the suppressive effects of PRL on GnRH release. Since the activation of alpha-adrenergic receptors increases hypothalamic CRH release, we evaluated whether PRL stimulates CRH release via an alpha-adrenergic mechanism. PRL stimulated basal CRH release by about twofold and this effect was inhibited by phentolamine in a concentration-dependent fashion. In conclusion, alpha-, but not beta-, adrenergic receptors mediate the inhibitory effects of PRL on GnRH release in vitro. We speculate that, at least under these experimental conditions, PRL inhibits GnRH release through an alpha-adrenergic mechanism which activates the CRH-secreting neurone.

Adrenergic alpha-Antagonists↗

PubMed1996

[Angiodysplasia of the right colon and aortic stenosis. A case report].

We report the case of a female patient who came to our observation for a severe enterorrhage. Following colonoscopic examination and color-Doppler M-B Mode echocardiography we made the following diagnosis: "angiodysplasia of the right colon in females with aortic stenosis". It was possible to ascertain whether there were similar lesions in other parts of the gastro-intestinal tract because the patient opposed firmly. In agreement with other authors, we believe that colonoscopic examination is the appropriate method to diagnose gastro-intestinal angiodysplasia. The advanced age and the clinical conditions of the patient did not allow surgical treatment, so we treated her with antihaemorrhagic drugs and elevated doses of ascorbic acid (4 g/die). The disappearance of enterorrhagies, the rapid clinical recovery and the normalization of red blood cell (RBC) count allowed us to discontinue antihaemorrhagic treatment and to continue the administration of elevated doses of ascorbic acid. Eight days later, the patient was discharged in good clinical condition and ascorbic acid was prescribed to be continued at home. A good clinical and haemodynamic balance was observed at the six-month follow-up. In conclusion we think that the clinical case we observed, characterized by the association angiodysplasia of the right colon-aortic stenosis, may be included in the diction Heyde's syndrome. In aging patients with severe concomitant diseases, ineligible for surgical interventions, the enterorrhage caused by a non complicated angiodysplastic lesion of the gastro-intestinal tract may benefit from the acute administration of ascorbic acid as the therapeutic agent of first choice capable to loose and/or stop the haemorragic complication and, in chronic administration, to reduce the number of relapses.

Aged↗

PubMed1995

[Role of MB-mode transthoracic echography in the early diagnosis of acute pulmonary embolism].

The aim of the present study was to evaluate whether transthoracic ecocardiography M-B mode was a sensitive and/or specific test for the early diagnosis of acute pulmonary embolism (PEA). For this purpose, we studied 7 patients with PEA as a complication of: deep leg venous thrombosis (3 cases), complicated bone fractures (2 cases), meniscectomy (1 case) and postpartum (1 case). The patients (3 males and 4 females), mean age of 46 +/- 7 years, did not have any previous earlier heart and/or pulmonary diseases. The diagnosis of PEA was made on the basis of clinical criteria, ecg and laboratory tests. Ecocardiography was performed using an IREX 3 M-B mode equipment; the measurements for the calculation of the indexes were made utilizing a short axis parasternal window. The parameters studied were: RVEDD/LVEDD ratio, LVDI Okubo index and the TR grade. Data were analyzed employing the paired Student's t test. In all patients was observed a statistically significant enlargement on the right heart cavities; while only in 3 of them was it possible to observe a slight reduction of the left ventricular cavities. In conclusion, the ecocardiographic exam was is a sensitive test for the diagnosis of PEA. Particularly, the RVEDD/LVEDD ratio gave an early and quantitative indication of the obstruction severity. Indeed, the morphological alteration of the right cavities became evident when the embolic obstruction was of at least 30%. Hence, we suggest that the standard ecocardiography M-B. mode may be regarded has a rapid diagnostic tool for the diagnosis of PEA.

Acute Disease↗

PubMed1991

Lyophilized collagen in the treatment of diabetic ulcers.

Diabetic foot ulcers are a significant clinical problem. Lyophilized type I collagen (LC) can stimulate wound healing by promoting platelet adhesion and aggregation and acting as a chemotactic factor for macrophages. The aim of the present study was to evaluate the efficacy of LC in the treatment of diabetic ulcers. Twenty patients (twelve males and eight females, age range 60-78 years) affected by non-insulin-dependent diabetes and ulcers (19 foot ulcers and 1 post-traumatic wrist ulcer) were, consecutively and at random, treated with LC or hyaluronic acid medicated gauze. The two groups were comparable in age, sex, size and etiopathogenesis of ulcers, metabolic state. The mean time for wound healing in the group treated with LC was 32.4 +/- 8.6 days, and in the group treated with hyaluronic acid medicated gauze was 49.0 +/- 11.0 days (p less than 0.001). The data suggest that LC significantly improves wound healing and is more active than medicated gauze in the treatment of diabetic ulcers.

Aged↗

PubMedDate not supplied

Acute lipidemic effect of calcium heparin in normolipemic and hyperlipemic subjects.

The Authors investigated the lipidometabolic effects of calcium heparin in order to assess if the antiatherogenic usefulness of the drug, recently demonstrated in the treatment of thrombosis and myocardial reinfarction, may be linked to its hypolipemiant property in addition to the antithrombotic one. The series consists of 25 normal-weight subjects (9 m, 16 f, mean age 68 +/- 5, RBW 107 +/- 3) of whom 11 were normolipemics (group A) and 14 hyperlipemics (group B) suffering from hyperlipoproteinemia of type IIA (4 cases), IIB (6 cases) and IV (4 cases). After an overnight fasting each subject was given calcium heparin (12,500 Units in a single dose subcutaneously); before and after 20', 1 hr, 2 hr and 6 hr venous blood samples were taken; for each sample plasma levels of triglyceride, total LDL-, total HDL-, HDL-3-, HDL-2-cholesterol, apoprotein CII, and apoprotein CIII were determined. In group A and B, triglycerides showed a significant reduction and total cholesterol a slight one, the "minima" being at the 1st hour after the heparinoid stimulus; the triglyceride reduction was more evident (8%) in group A than in group B (17%). In group A, total HDL-, HDL-2- and HDL-3-cholesterol decreased significantly (P less than 0.01) with a "nadir" at the 2nd hr in group B; total HDL-cholesterol did not change, whereas HDL-3-cholesterol decreased (P less than 0.05) and HDL-2 cholesterol increased (P less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗

PubMedDate not supplied

Lipidemic effects of a mild-term treatment with calcium heparin in vasculopathic subjects.

The Authors study the lipidemic effects of a "middle-term" treatment with heparin calcium in vasculopathic subjects undergoing the drug for antithrombotic purposes. The series consists of 35 subjects (21 m, 14 f, mean age 57 +/- 8) suffering from peripheral arteriopathy (24 cases) and instable angina (11 cases) of arteriosclerotic nature, and free from endocrinometabolic and hepatorenal diseases; all the subjects were normolipemic, except for 4 cases having hyperlipoproteinemia of type II B. After a week of standard diet and drug wash-out, each patient underwent antithrombotic treatment with calcium heparin (10.000 Units subcutaneously) for three weeks during the hospitalization; for each sample, the plasma levels of triglycerides (TG), total cholesterol (TC), LDL-cholesterol (LDL-C), HDL-cholesterol (HDL-C), HDL-3-cholesterol (HDL-3-C) and HDL-2-cholesterol (HDL-2-C) were determined enzymatically (kits Boerhinger Mannheim). The Authors observe a significant (P less than 0.05) increase of TC and LDL-C after one and after two weeks of treatment with a return to the baseline after three weeks; levels of TG, HDL-C, HDL-3-C, HDL-2-C and the HDL-C/TC and HDL-2-C/HDL-C ratios showed an ascending profile until the third week without significant changes, compared to the baseline values. Subdividing the series arbitrarily into into two groups (A and B) respectively having rather low ("normolipemic") and high ("hyperlipemic") values of TC and TG respectively below (group A) and above (group B) 230 mg/dl (TC) and 165 mg/dl (TG).(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗

PubMedDate not supplied

Left ventricular performance after intravenous infusion of captopril in patients with congestive heart failure.

BACKGROUND: Although oral administration of captopril, an angiotensin-converting enzyme inhibitor, is effective for the treatment of congestive heart failure (CHF), the effect of its intravenous (iv) administration is not well known. METHODS AND RESULTS: Ten patients (age range 48-72 years), with CHF belonging to the second and third NYHA class, were given an iv bolus of 25 mg of captopril. Before and 30 minutes after the infusion of captopril, a number of parameters of the left ventricular function were evaluated by echocardiography IREX 3 M-B Mode. Eight patients showed a significant improvement of left ventricular performance indices. In fact, the ejection fraction (13.8%, p < 0.05), the cardiac output (24%, p < 0.001), the circumferential shortness fraction (29.9%, p < 0.05), and the fraction shortening (16.0%, p < 0.005) increased significantly, whereas the end-systolic diameter (21%, p < 0.001), the endsystolic stress (23.8%, p < 0.01) and the left ventricle ejection time (4.8%, p < 0.05) decreased significantly. Systolic and diastolic blood pressure values also underwent a significant reduction by 17% and 11% (p < 0.01 and p < 0.05 respectively). No evident correlation between the improvement of the left ventricular function and the basal renin rates was noticed. CONCLUSIONS: A significant improvement of parietal kinesis was observed especially in those segments which showed movement abnormalities (hypokinesia and akinesia) and in many cases this was detected by M-B Mode echocardiography. Our findings may be the result of the following factors: 1) reduction of parietal stress; 2) increased district coronary flow; 3) inhibition of tissue renin-angiotensin-aldosterone system; and 4) "scavenging" action exerted by the SH group of captopril.

Aged↗