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Biomedical subjects

G Segre

Publications and source records attributed to G Segre.

At least 55 records · Page 3Linked to original sources
PubMed1985

Effect of ACTH, beta-endorphin, morphine and naloxone on the release of cortisol by isolated adrenal glands.

The release of cortisol (determined by RIA) from isolated slices of adrenal glands of guinea pigs is stimulated by ACTH, by beta-endorphin, and by morphine in a concentration-dependent way; naloxone gives a small stimulation which is not related to its concentration. Naloxone inhibits the effect of ACTH (1.11 X 10(-11) M) in a competitive manner with an IC50 of about 3.10(-9) M. Also morphine and beta-endorphin inhibit the effect of ACTH, but not in competitive manner. Naloxone (10(-9)-10(-7) M) gives a concentration-related inhibition of the increase of cortisol release produced by morphine (10(-8) M) and by beta-endorphin (1.44 X 10(-10) M). These data suggest a similarity in the conformation of ACTH, beta-endorphin, morphine and naloxone towards the binding sites of ACTH of the guinea pig adrenal glands.

Adrenal Glands↗
PubMed1985

Effect of morphine and naloxone on the levels of ACTH and beta-endorphin in plasma, brain and pituitary of rats.

The effect of i.p. administration of morphine (25 mg/kg) and of naloxone (50 mg/kg) on the levels of ACTH and beta-endorphin in plasma, in brain and in pituitary has been studied in rats. An opposite effect morphine and naloxone is seen in plasma ACTH with an increase elicited by morphine and a decrease produced by naloxone. Small changes are seen in plasma levels of beta-endorphin as well as in ACTH and in beta-endorphin levels in brain and in pituitary. To every change in ACTH levels in plasma an opposite change in ACTH brain levels is observed.

Adrenocorticotropic Hormone↗
PubMed1985

Pharmacokinetics of flunitrazepam in rats studied by a radioreceptor assay.

In rat the kinetics of flunitrazepam (FNZ) was evaluated by a radioreceptor assay (RRA) after i.v. administration of 1 mg/kg and after oral administration of 1 and 3 mg/kg. The i.v. kinetics is biexponential and the g.i. absorption is very rapid (with a plasma peak at 0.25 hour) with a good bioavailability (69%); the apparent distribution volume is high, 4.8 L/kg; the half-life is equal to 3.5 hours; the elimination constant is equal to 0.8 h-1; the urinary excretion of FNZ-equivalent is negligible; the plasma total clearance is equal to 3.9 (L/kg)h-1. The concentrations of FNZ-equivalents after oral administration of 1 mg/kg show a peak at the 2-nd hour with a very high concentration in the following organs (in decreasing order): brain, kidneys, heart, liver; after 8 hours no FNZ-equivalents are present in these organs except in the brain, which shows detectable concentrations at the 32-nd hour. The peak concentrations of FNZ-equivalent in brain, kidneys and heart are higher than the corresponding peak concentration in plasma.

Animals↗
PubMed1985

The kinetics in the rat of a new nitroimidazole derivative.

A new nitroimidazole derivative, N-(5-carboxy-5-amino pentane) carbamic ester of 1(2-hydroxyethyl)-2-methyl-5-nitroimidazole (APMN), was administered to rats by the following routes: i.p. and orally (100 mg/kg); i.m. (100 and 250 mg/kg). Plasma kinetics of the drug fit a monoexponential function with a half-life of 0.5 h and a volume of distribution of 555 ml/kg. In tissues the peak levels of the drug (at 0.5 h) were 700, 150 and 40 micrograms/g in kidney, liver and heart respectively and their disappearance rate was similar to that observed for plasma. Urinary excretion of the unmodified drug in 23 h was less than 30% of the administered dose. No APMN was found in plasma and urine after oral administration.

Animals↗
PubMed1985

Aspects of the mechanisms of action of benzydamine.

Benzydamine shows some properties that are common with other nonsteroidal antiinflammatory drugs (NSAIDs) but displays also properties which are different from those of other NSAIDs. It inhibits prostaglandin and thromboxane biosynthesis at high concentrations, which however can be reached by topical application of the drug. It has no inhibiting effect on amino-acid decarboxylases, which are inhibited by various NSAIDs. Benzydamine has no effect on sulphydryl-group reactivity, contrary to most NSAIDs. It inhibits platelet aggregation and the inhibition of the collagen-induced aggregation appears to be rather selective with respect to other NSAIDs. It displays a stabilizing effect on erythrocyte membranes which appears related to its high affinity for membranes in general, and it inhibits the respiratory burst of stimulated human monocytes and granule enzyme release by human neutrophils.

Animals↗
PubMed1984

Plasma kinetics of dihydroergotoxin in rat by using a radioreceptor assay.

A radioreceptor assay (RRA) (with brain dopamine receptors) has been developed to determine the levels of dihydroergotoxin-equivalent (DHT-equivalent) material in rat plasma and its kinetics after oral and i.v. administration (5 mg/kg). After i.v. administration the plasma kinetics follows a two-exponential equation, with an apparent distribution volume of 7-9 1/kg and a long half-life (about 36 hours). The kinetics of DHT after oral administration shows two peaks; this could indicate a biliary recycling of the drug and/or of its metabolites. The low bioavailability (19%) and the biliary recycling of DHT-equivalent material suggest a first pass effect.

Administration, Oral↗
PubMed1984

Pharmacokinetic study on intravenous rifampicin in man.

A pharmacokinetic study was carried out in 18 male patients in order to assess the blood concentrations of rifampicin after intravenous administration of 3 different doses (600, 900 and 1200 mg) over 3 different periods of infusion (1, 2 and 3 hours). The results show that, by increasing the dose and the rate of infusion higher and earlier peak concentrations are obtained. A kinetic analysis based on a one-compartment open model gives a good fitting of the data obtained experimentally. From these data one obtains for the volume of distribution a value of 48.1 +/- 17.2 liters and for the serum disappearance rate the value of 0.212 +/- 0.070 h-1 in adult subjects. It is possible to predict the time course of serum kinetics of the drug by using the equation (formula; see text).

Bilirubin↗
PubMed1984

Inhibition of aminoacid decarboxylases by non-steroidal antiinflammatory drugs.

Several non-steroidal antiinflammatory drugs (NSAID) were shown to inhibit to various extents the decarboxylases of ornithine, lysine, histidine, arginine, and tyrosine. The most sensitive enzyme was ornithine decarboxylase, for which piroxicam, benoxaprofen and aminophenazone showed an IC50 of 0.007 mM; ibuprofen competitively inhibits the lysine decarboxylase. The most effective NSAID's in inhibiting histidine decarboxylase were mefenamic acid, ibuprofen and flufenamic acid. Arginine and tyrosine decarboxylase were inhibited by NSAID's only at high concentrations. None of the decarboxylase inhibitions were reversed by pyridoxal phosphate. Subplantar injection of the 5 amines formed by these aminoacid decarboxylases elicited a paw oedema in rat which was not antagonized by the various NSAID's. Some of the NSAID's stimulated all the decarboxylases and did not antagonize the carrageenin-induced paw oedema. With one exception, all the NSAID's tested in vivo inhibited the elimination of 14CO2 from labeled ornithine and lysine. The inhibition of certain aminoacid decarboxylases, particularly ornithine and lysine decarboxylase, appears to be a noteworthy mechanism of action for certain NSAID's.

Animals↗
PubMed1983

Kinetics of ouabain outflow from isolated frog heart evaluated by the dose-effect relationship and compared to the outflow kinetics of the tritiated drug.

In isolated frog hearts the kinetics of ouabain disappearance from the receptor biophase(s) related to the effect has been calculated from the relationship between ouabain concentration and its inotropic effect. When 10(-4) - 10(-5) M ouabain is added to the heart, the kinetics is biexponential with a fast component with a time constant of 1.7 min-1 and a slower component with a time constant of 0.28 min-1. The kinetics of the washout curve of 3H ouabain (added together with unlabelled drug, shows, in addition to the slow exponential component of about the same time constant (0.2 min-1) previously seen, another component with a 10 times longer time constant, related to ineffective drug concentrations and corresponding to a washout from aspecific sites. The kinetics of ouabain outflow from compartments which are related to the effect elicited by 10(-4) - 10(-5) M concentrations is formed mainly by two steps with time constants of 1.7 min-1 and 0.28 min-1.

Animals↗
PubMed1983

Indomethacin and sulindac inhibition of ACTH stimulated cortisol release from adrenal glands in vitro.

In slices of adrenal glands of guinea pig added ACTH (from femtograms to picograms levels) stimulates cortisol synthesis and release. This effect is antagonized in a non-linear competitive way by indomethacin (KE = 1.3 .10(-7)) and by sulindac (KI = 6.9 .10(-10)); indoprofen is a very weak antagonist. A number of other non-steroid antiinflammatory drug are ineffective as antagonists of ACTH.

Adrenal Glands↗