Search PubMed⌕ Search

Biomedical subjects

S Amoroso

Publications and source records attributed to S Amoroso.

At least 55 records · Page 3Linked to original sources
PubMed1988

Antigens of Euparipha pisana (snail). I. Identification of allergens by means of in vivo and in vitro analysis.

The data obtained in this study suggest that eating Euparipha pisana (snail), a common food in Mediterranean countries, could give serious allergic reaction such as asthma. We describe here the identification and partial characterization of allergenic molecules form this new source. An aqueous extract of snail was obtained by homogenization in distilled water, centrifugation, dialysis and defatting with ethyl ether. Skin prick test (SPT) performed with the snail extract on 70 subjects allergic to the more common allergens of the Mediterranean area gave a SPT positivity in 61% of the subjects tested, with a mean value of histamine-equivalent prick (HEP) equal to 0.81 +/- 0.25 (n = 43), while no SPT-snail-positive reactions were obtained by using the same extract on 30 not allergic subjects. To ascertain if such a sensitivity was IgE-mediated, sera from SPT-snail-positive subjects were analyzed by RAST, coupling the snail extract to polystyrene balls and to paper discs. 19% of the sera tested were RAST-positive, mean value of binding 4.8 +/- 2.8% (n = 13), while when using sera from SPT-snail-negative subjects, the RAST mean value was 0.49 +/- 0.18% (n = 27). Histamine release (HR) was also performed. Basophils prepared from SPT-snail-positive subjects were incubated with a snail extract. All of the SPT-snail-positive subjects gave a significant value of HR, mean value 21.8 +/- 7% using 1 micrograms of snail extract (n = 16), while 1.41 +/- 1.1% (n = 10) was the mean value obtained when SPT-snail-negative subjects were analyzed.(ABSTRACT TRUNCATED AT 250 WORDS)

Allergens↗
PubMed1988

Membrane events and ionic processes involved in dopamine release from tuberoinfundibular neurons. I. Effect of the inhibition of the Na+,K+-adenosine triphosphatase pump by ouabain.

In the present study we investigated the membrane events and the ionic processes which mediate the stimulatory effect of ouabain on the release of endogenous dopamine (DA) and "previously taken-up" [3H]DA release from rat hypothalamic tuberoinfundibular dopaminergic (TIDA) neurons. Ouabain (0.1-1 mM) dose-dependently stimulated endogenous DA and "newly taken-up" [3H]DA release. This effect was counteracted partially by nomifensine (10 microM). Removal of Ca++ ions from the extracellular space in the presence of the Ca++-chelator ethylene glycol bis(beta-aminoethyl ether)-N,N'-tetraacetic acid prevented completely ouabain-elicited [3H]DA release. Lanthanum (1 mM) and cobalt (2 mM), two inorganic Ca++-entry blockers, were able to inhibit this stimulatory effect, whereas verapamil (10 microM) and nitrendipine (50 microM), two organic antagonists of the voltage-operated channel for Ca++ ions, failed to affect ouabain-induced [3H]DA release. By contrast, adriamycin (100-300 microM), a putative inhibitor of cardiac Na+-Ca++ antiporter, dose-dependently prevented ouabain-induced [3H]DA release from TIDA neurons. Finally, tetrodotoxin reduced digitalis-stimulated [3H]DA release. In conclusion, these results seem to be compatible with the idea that the inhibition of Na+,K+-adenosine triphosphatase by ouabain stimulates the release of [3H]DA from a central neuronal system like the TIDA tract and that this effect is critically dependent on the entrance of Ca++ ions into the nerve terminals of these neurons. In addition the Na+-Ca++ exchange antiporter appears to be the membrane system which transports Ca++ ions into the neuronal cytoplasm during Na+,K+-adenosine triphosphatase inhibition. The enhanced intracellular Ca++ availability triggers DA release which could occur partially through a carrier-dependent process.

Animals↗
PubMed1988

Membrane events and ionic processes involved in dopamine release from tuberoinfundibular neurons. II. Effect of the inhibition of the Na+-Ca++ exchange by amiloride.

In the present study we investigated the effect of amiloride, a rather specific inhibitor of the membrane Na+-Ca++ exchange system, on the release of endogenous dopamine (DA) and "previously taken-up" [3H]DA from tuberoinfundibular dopaminergic neurons. Amiloride (300 microM) stimulated either endogenous DA or [3H]DA release. Amiloride-induced stimulation of [3H]DA release was prevented in a Ca++-free plus ethylene glycol bis(beta-aminoethyl ether)-N,N'-tetraacetic acid medium. Amiloride, at the same concentration, reinforced both high K+- and electrically-induced stimulation of [3H]DA release. These results are explained on the basis of the ability of amiloride in blocking the Na+-Ca++ exchange system, therefore causing an elevation of intracellular Ca++ levels in resting conditions, and a further accumulation of Ca++ ions after high K+- or electrically elicited opening of voltage-operated channels specific for Ca++ ions. The enhanced intracellular Ca++ availability may trigger the stimulation of neurotransmitter release. In addition, amiloride was able to block in a dose-dependent manner (70-300 microM) the ouabain-induced [3H]DA release, suggesting that, when intracellular concentrations of Na+ are increased by the blockade of Na+,K+-adenosine triphosphatase the Na+-Ca+;+ exchange carrier reverses its resting mode of operation, mediating the influx of extracellular Ca++ ions. Amiloride, by blocking the Na+-Ca++ exchange mechanism, prevents the ouabain-elicited entrance of extracellular Ca++ ions, therefore inhibiting [3H]DA release stimulated by the cardioactive glycoside. Collectively, the results of the present study seem to be compatible with the idea that the Na+-Ca++ exchange mechanism is involved in the regulation of [3H]DA release from tuberoinfundibular dopaminergic neurons, through the regulation of Ca++ movements across the plasma membrane.

Amiloride↗
PubMed1987

Domperidone antagonizes bromoergocriptine--induced nausea and vomiting without affecting its inhibition of prolactin secretion in puerperal women.

In the present study, 122 post puerperal women received at random bromoergocriptine, domperidone, bromoergocriptine plus domperidone or placebo treatment. Domperidone started 20-24 h after delivery and given for 10 or 15 days did not antagonize either the decrease in serum PRL induced by bromoergocriptine or the inhibition of lactation. It did suppress nausea and vomiting in the patients. The results are compatible with the idea that domperidone binds with a higher affinity than bromoergocriptine to DA (dopamine) receptors in the area postrema or the stomach. The converse phenomenon occurs at the level of the DA receptors on the PRL- secreting cells of the anterior pituitary gland.

Adult↗
PubMed1987

Possible inhibitory role of histamine H2 receptors in the control of basal TSH secretion in male rats: studies with dimaprit, a selective H2 receptor agonist.

Dimaprit,a selective H2 receptor agonist, induced a dose-related decrease of serum TSH basal levels in male rats. This effect was blocked in animals pretreated with cimetidine, a blocker of H2 receptors. Furthermore, dimaprit, added to the anterior pituitary in vitro, failed to induce any change of TSH release. These results are consistent with the hypothesis of an inhibitory role played by H2 receptors located on the median eminence in the control of TSH secretion in male rats.

Animals↗
PubMed1986

Maitotoxin and Bay-K-8644: two putative calcium channel activators with different effects on endogenous dopamine release from tuberoinfundibular neurons.

In the present study we report on the effects of two putative calcium channel activators, maitotoxin and the dihydropyridine BAY-K-8644, on endogenous dopamine release from tuberoinfundibular dopaminergic neurons. Maitotoxin stimulated basal dopamine release and this effect was calcium-dependent. By contrast BAY-K-8644 failed to produce any modification of basal or high potassium-induced dopamine release. These results suggest that maitotoxin, unlike BAY-K-8644, represents a suitable tool to investigate the functional role of calcium channels in central dopaminergic neurons.

3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethy↗
PubMed1986

Reduced tuberoinfundibular dopaminergic neuronal function in rats after long-term withdrawal of estrogen treatment.

Hypothalamic fragments from female rats treated repeatedly with estradiol valerate (EV) and bearing prolactin (PRL)-secreting tumors contained, seven months after the last EV injection, lower concentrations of dopamine (DA) than age-matched controls. Depolarizing concentrations of K+ (35 mM) and amphetamine (50 microM) evoked in PRL-secreting tumor bearing rats an endogenous DA release significantly lower than in controls.

Animals↗
PubMed1986

Endogenous dopamine release from tuberoinfundibular neurons: does calmodulin play any role?

The possible involvement of calmodulin in the process of endogenous dopamine (DA) release from arcuate-periventricular nuclei-median eminence fragments, containing tuberoinfundibular dopaminergic (TIDA) neurons, has been investigated in an in vitro incubation system. For this purpose the basal and K+-stimulated DA release was examined in the presence and in the absence of the different putative calmodulin antagonists, pimozide, trifluoperazine, penfluridol and N-(6-aminohexyl)-5-chloro-1-naphthalenesulfonamide (W-7). Trifluoperazine and pimozide in concentrations up to 100 microM were both uneffective in blocking K+-evoked DA release. Penfluridol in doses of 5 and 10 microM, did not prevent 35 mM K+-induced endogenous DA release. It was able to reduce K+-stimulated DA release only at the very large concentration of 100 microM. W-7 added in vitro to the hypothalamic fragments, prevented endogenous DA release evoked by 35 mM K+ in a dose-dependent manner. W-5, a chlorine deficient analogue of W-7, that interacts only weakly with calmodulin, failed to modify K+-stimulated endogenous DA release in doses up to 200 microM. All the putative calmodulin antagonists used in the present study did not induce any change of basal DA release. In conclusion the fact that most of the agents, except W-7, known to antagonize calmodulin-dependent processes in many biological systems failed to interfere with the release of endogenous DA from TIDA neurons seems to suggest that calmodulin does not play a crucial role in the process of DA release and that the inhibitory effect of W-7 on endogenous DA release may be better attributed to other mechanisms different from its anticalmodulin action.

Animals↗
PubMed1986

Effect of different organic and inorganic blockers of calcium entry on the release of endogenous dopamine from tuberoinfundibular neurones.

In the present study the effect of different blockers of calcium entry belonging to different chemical classes on basal and K+-elicited release of endogenous dopamine (DA) from tuberoinfundibular dopaminergic neurones was studied in vitro. For this purpose fragments of hypothalamus containing arcuate-periventricular nuclei and median eminence were incubated in vitro and endogenous DA released into the medium was assayed by radioenzymatic assay. The organic blockers of calcium entry, nitrendipine, nimodipine, nifedipine, diltiazem and flunarizine did not modify basal or K+-evoked release of endogenous DA, unless very large concentrations (100 microM) of nifedipine or diltiazem were used. The phenylalkylamine methoxyverapamil (D-600) consistently inhibited K+-stimulated release of endogenous DA in concentrations of 50 and 100 microM. Cobalt and lanthanum, two ions with an ionic radius similar to that of calcium and which are known to inhibit calcium fluxes through nerve membranes, significantly blocked release of endogenous DA elicited by 35 mM K+. In summary, the results of the present study showed that calcium channels in the tuberoinfundibular dopaminergic system displayed a different sensitivity to various classes of blockers of calcium entry. Inorganic blockers of calcium entry, like lanthanum and cobalt, appeared to be the most effective in blocking Ca2+-dependent release of endogenous DA, whereas, among the organic calcium antagonists, phenylalkylamines seemed to possess a certain degree of effectiveness.

Animals↗
PubMed1984

Dual effect of verapamil on K+-evoked release of endogenous dopamine from arcuate nucleus-median eminence complex.

The effect of verapamil, a calcium-entrance blocker, on K+-evoked release of endogenous dopamine from tuberoinfundibular neurons incubated in vitro was studied. This compound, added to the incubation medium, at the dose of 10(-6) M, significantly reinforced K+-induced dopamine release, whereas, at higher doses (10(-5), 5 X 10(-5) and 10(-4) M), it completely prevented the stimulated dopamine release. The results obtained with the higher doses showed the calcium dependence of K+-evoked release of endogenous dopamine from central neurons. The opposite effect, seen with the lower dose of verapamil, could be due to different pharmacological properties of the drug.

Animals↗
PubMed1984

Release of endogenous dopamine from tuberoinfundibular neurons.

Release of endogenous dopamine(DA) from arcuate-periventricular nucleus-median eminence fragments has been analyzed in an in vitro static incubation system. Exposure of these hypothalamic fragments to increasing concentrations of K+ ions produced a dose-dependent release of endogenous DA. The highest rate of K+-stimulated DA efflux occurred in the first 10 minutes, thereafter it progressively declined reaching prestimulated levels at 30 minutes. If two consecutive depolarizing stimuli of 40 mM KCl were applied to the same hypothalamic fragment, after a 40 minutes rest period, an equivalent release of endogenous DA occurred. Removal of Ca++ ions from the incubation medium containing the Ca++ chelator EGTA caused a decrease of basal DA efflux and completely prevented the K+-induced release of DA. Furthermore when verapamil, a blocker of Ca++ entrance, was added to the incubation medium in a concentration of 50 microM, the K+-induced DA efflux was completely counteracted, whereas spontaneous release was unmodified. Finally nomifensine, a potent blocker of DA uptake, added in vitro in a final concentration of 10 microM, significantly reinforced K+-induced release of endogenous DA. Since nomifensine did not modify basal DA release, this study confirmed its prevalent uptake blocking property rather than its releasing action on DA.

Animals↗
PubMed1984

Applicability of a simple nasal provocation test in etiologic diagnosis of bronchial asthma.

The applicability of nasal challenge for etiologic diagnosis of extrinsic asthma was evaluated by assessing easiness of performance, precision, and cost of a standardized test by metered nebulizer in 20 asthmatics with and without concurrent rhinitis submitted also to skin prick tests and RAST. Although less sensitive than in the group with rhinitis (where precision was 90.4%), the nasal provocation test proved to be an easy, inexpensive, and specific (82.3%) means for contributing to the identification of allergic sensitization in patients affected by asthma alone.

Administration, Intranasal↗
PubMed1983

Increased GH responsiveness to dopamine receptor stimulation in alcohol addicts during the late withdrawal syndrome.

In humans the release of growth hormone (GH) elicited by dopamine (DA) and DA agonists may represent a reliable model to assess change in sensitivity of DA receptors. We now report that in chronic alcoholics, 4-7 days after the suspension of alcohol consumption, the increase of GH response to DA infusion was higher than that seen in non alcoholic volunteers. The specificity of this GH response to DA administration was demonstrated by the use of domperidone, a novel peripheral antagonist of DA receptors. These results suggest the development of hyper-responsiveness of DA receptors involved in the control of GH secretion in chronic alcoholics during the later phases of the "withdrawal syndrome".

Adult↗
PubMed1983

[Effects of dimaprit, an H2 receptor agonist, on blood levels of corticosterone in the rat].

These experiments were performed in order to further clarify the role played by hystamine in the control of hypothalamus-hypophisis-adrenal axis. To this aim we evaluated the effect of Dimaprit, a H2 agonist on plasma corticosterone levels. This drug was administered intraperitoneally or i.c.v. at the doses of 25, 50 and 100 mg/kg or 100 gamma/animal respectively. The administration i.p. at the dose of 100 mg/kg increased plasma-corticosterone levels whereas Dimaprit, injected intraventricularly did not modify plasma-corticosterone levels. These results seem to suggest that Dimaprit stimulates corticosterone secretion at a peripheral level.

Animals↗
PubMed1983

Analysis of dose-response curves in the detection of bronchial hyperreactivity.

In 12 reference subjects and 23 asthmatic patients under clinical and functional remission, dose-response curves following inhalation of nebulized carbachol solution were performed. Response was assessed both in terms of SRaw and SGaw and the best fitting mathematical function (linear, exponential, polynomial and logarithmic) was looked for. Discriminating power and day-to-day reproducibility were better when using SGaw, independently from the fitted model. For the sake of simplicity, therefore, the linear or exponential treatment of indices seem preferable.

Adult↗