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Biomedical subjects

G De Natale

Publications and source records attributed to G De Natale.

At least 37 records · Page 2Linked to original sources
PubMed1991

[Cadmium-induced changes in the activity of the dopaminergic and purinergic systems and in ascorbic acid catabolism in the rat striatum].

Levels of dopamine (DA), 3-4-dihydroxyphenylacetic acid (DOPAC), ascorbic acid (AA), dehydroascorbic acid (DHAA), uric acid (UA) and adenosine (ADO), were determined by HPLC in the striatum of male Wistar rats treated with repeated injections of cadmium (as sulfate) 3 mg/kg/day s.c. for 10 consecutive days. Cadmium treatment significantly reduced DOPAC levels with consequent decrease of the DOPAC/DA ratio; AA levels were significantly reduced, while DHAA levels were significantly increased, with consequent increase of DHAA/AA ratio: levels of UA and ADO were both significantly increased. It is concluded that cadmium, given systemically, reduces dopaminergic system activity in the rat striatum; such impairment occurs together with an increase of AA oxidation and of markers of purinergic system activity. The inhibition of striatal dopaminergic activity could be considered the neurochemical basis of behavioral changes induced by cadmium, while the increase of AA oxidation and of purinergic system activity could be considered an antitoxic metabolic response.

Adenosine↗
PubMed1991

Analysis of the mechanism of d-amphetamine-and apomorphine-induced changes of ascorbic acid catabolism in discrete brain areas of the rat.

Ascorbic acid (AA) levels and dehydroascorbic acid/ascorbic acid (DHAA/AA) ratios were determined in hypothalamus, striatum, and remaining brain of male Wistar rats, after single or repeated injections of d-amphetamine (1.8 mg/kg/day s.c.), apomorphine (1.0 mg/kg/day s.c.), and/or haloperidol (0.1 mg/kg/day i.p.). Major changes were observed in hypothalamus, in which all drugs significantly increased DHAA/AA ratio. Apomorphine and haloperidol consistently decreased AA level as well. The DHAA/AA ratio increase was observed also when apomorphine and d-amphetamine were associated with haloperidol. In striatum, apomorphine (single) and d-amphetamine (repeated) injections increased DHAA/AA ratios; such AA oxidation increase was inhibited by haloperidol; the increases (d-amphetamine) or decrease (apomorphine) of AA levels were also inhibited by haloperidol; haloperidol alone did not modify DHAA/AA ratio and induced minor changes of striatal AA level. In remaining brain, apomorphine (single) and d-amphetamine (repeated) treatment increased DHAA/AA ratio; such increase was observed also when haloperidol was associated with apomorphine or d-amphetamine; moreover, haloperidol by itself increased AA oxidation, although to a lesser extent than it did in hypothalamus. It is concluded that AA catabolism can be activated in the rat striatum by a dopaminergic mechanism; in hypothalamus and in remaining brain, the AA catabolism activation appears rather to be a non-specific effect of the pharmacological manipulation.

Animals↗
PubMed1990

[Cardiotoxicity of emetine].

Emetine is still an important agent for the treatment of invasive intestinal amebiasis and amebic liver abscess. Its most relevant side effect is its well documented cardiotoxicity. The authors review the hypotheses that have been suggested concerning the mechanism of this cardiotoxic action.

Animals↗
PubMed1990

[Drugs interfering with platelet function].

Drugs interfering with platelet aggregation pathways and Ca2+ availability were reviewed. Particularly receptor antagonists, drugs affecting intracellular concentration of cAMP and drugs acting on enzymes involved in the synthesis of PGE2 and PGF2, thromboxane and PGI, were considered.

Blood Coagulation Factors↗
PubMed1989

[Drugs used in the therapy of peptic ulcer with special reference to H2 receptor blockaders].

Drugs used in the management of peptic ulcer are reviewed with special attention to the possibilities offered by H2 receptor antagonists. In this context, histaminergic transmission and distribution of H2 receptors are briefly reviewed. Among other substances, special interest has been raised by H+ and K+-dependent ATPase inhibitors; the most recently introduced derivatives of these substances which are as yet in the experimental stage, are also listed.

Antacids↗
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↗
PubMed1980

Cimetidine and adrenals.

An H2-antagonist, cimetidine, reduces in the rat normal plasma corticosterone levels and strongly antagonizes their increase after cold stress. This latter effect is dose dependent. Plasma corticosterone reduction by cimetidine lasts 4 h both in normal and stress situations. Both a hypophyseal or adrenal site of action of the drug may be involved in the inhibition of adrenocortical secretion.

Adrenal Glands↗