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Biomedical subjects

J Mardones

Publications and source records attributed to J Mardones.

At least 19 recordsLinked to original sources
PubMed1989

[Scientific research: a cultural legacy].

This is the conference given by Jorge Mardones, Emeritus Professor of the University of Chile on the occasion of receiving the Juvenal Hernández award. A biographical trace of Professor Mardones scientific career and its motivations, including his relation to outstanding Chilean scientists is included. A remembrance of Juvenal Hernández, former rector of this University is offered.

Chile↗
PubMed1985

Effects of diets decreasing ethanol consumption on acetaldehyde metabolism in UChA and UChB rats.

It has previously been reported that the introduction of a new issue (D1) of a stock diet (D0) caused a significant decrease in voluntary ethanol consumption in rats of our UChA (low ethanol consumer) and UChB (high ethanol consumer) strains, and that, after changing to a diet lacking in animal products (D3), ethanol consumption reached the previous level attained in UChB rats and exhibited a bimodal distribution in UChA rats in such a way that about one-third of these consumed more than 2 ml of a 10% (v/v) ethanol solution per 100 g of body weight, as did UChB rats. When UChA rats exhibiting high ethanol consumption and also UChB rats were fed on the D3 diet with a brewer's yeast supplement, a significant decrease in ethanol intake was observed. Since significant correlations of voluntary ethanol intake to blood acetaldehyde levels, and to hepatic and brain aldehyde dehydrogenase (AldDH) activities, have been reported, the effects on these parameters of diet D1 and of supplements of brewer's yeast or disulfiram were studied. Results showed that rats of both strains fed on a D1 diet exhibited a significant increase in blood acetaldehyde level after ethanol administration, concomitant with an inhibition of hepatic and brain AldDH activities and a significant decrease in ethanol intake. Thus, this effect could be related to a disulfiram-like activity. The decrease in ethanol intake induced by brewer's yeast was not accompanied by changes of blood acetaldehyde level after ethanol, nor by inhibition of hepatic AldDH activity in either strain.(ABSTRACT TRUNCATED AT 250 WORDS)

Acetaldehyde↗
PubMed1984

Effects of different diets on voluntary consumption of ethanol in UChA and UChB rats.

Based on the decrease of voluntary consumption of ethanol observed in rats of UChA (low ethanol consumer) and UChB (high ethanol consumer) strains, coincident to the use of a new issue of a commercial diet, the effects of two new diets devoid of animal food were studied. One of these diets (Diet 3) induced an increase of the voluntary consumption of ethanol in a proportion of UChA rats, in such a way that its frequency distribution curve resulted in a bimodal one because of the presence of individuals which drank as much alcohol as UChB rats. This diet is a useful tool for the study of eventual nutrimental factors which decrease ethanol intake.

Alcohol Drinking↗
PubMed1984

Biological similarities and differences between rats genetically different in alcohol preference.

This paper is an inventory of some behavioural, biochemical and pharmacological similarities and differences between two inbred strains of Wistar rats differing in voluntary consumption of ethanol, namely: UChA and UChB with low and high preferences respectively for ethanol under conditions involving free choice between a 10% (v/v) ethanol solution and distilled water. The following strain differences were observed: ethanol consumption (UChA less than UChB); total water consumption (UChA less than UChB); solid food consumption (UChA greater than UChB); rate of recovery of ethanol label in expired CO2 (UChA less than UChB); oxidation of ethanol to acetaldehyde by brain homogenates (UChA greater than UChB); acetaldehyde disposal by brain homogenates (UChA less than UChB); ethanol (90 mmol/kg, i.p.) sleeping-time (UChA less than UChB); chronic and acute tolerance to ethanol (UChA developed it, whereas UChB did not); lethal doses of ethanol (UChA greater than UChB); recovery rate of the label of gluconate in expired CO2 (UChA less than UChB); recovery rate of the label of fructose in expired CO2 (UChA less than UChB); blood-glucose level after glucose (1 g/kg, i.p.) load (UChA less than UChB). No strain differences were observed in the rate of recovery in expired CO2 of the label of the following substrates: acetate, pyruvate, butyrate, citrate, ribose, glycerol, sorbitol, glucose and galactose.

Alcoholic Intoxication↗
PubMed1976

Receptors for morphine and opioids.

Two points concerning enzymatic systems acting on disposal of morphine are discussed, namely the multiplicity of glucuronyltransferase and the effect of nalorphine on N-demethylation of morphine. Evidences of the presence of at least two different glucuronyltransferases in microsomes of rat liver, kidney and intestine are presented. These evidences are given by the different distribution of the glucuronizing activity for morphine and rho-nitrophenol in microsomal preparations of these organs; by the different glucuronidation activity for both substrates induced by phenobarbital and 3-methylcholantrene; and finally by the chromatographic separation of fractions with enzymatic glucuronidating activity only for rho-nitrophenol or only for morphine. Nalorphine in concentrations of 1.3 X 10(-3) M and 1.3 X 10(-4) M inhibited in vitro de-N-demethylation of morphine 1.3 X 10(-3) M by the supernatant of rat liver homogenates, while in concentration of 1.3 X 10(-5) M it enhanced this reaction.

Age Factors↗
PubMed1975

Studies on the mechanism of the action of morphine on the peristalsis of guinea pig ileum in situ.

The influence of some drugs on the effect of morphine on the threshold pressure required to elicit peristalsis in the guinea pig ileum in situ was studied, in order to test the hypothesis that this effect of morphine is mediated by catecholamine release. Tachyphylaxis to this effect of morphine was confirmed. Pretreatemnt with two 8 mg/kg doses of reserpine, 24 and 48 hrs before the experiment, significantly reduced the effect of morphine on the pressure threshold. The i.v. administration of 10 mg/kg dl-Dopa re-established the effect of morphine in reserpinized animals to the level of the untreated controls. Pretreatment with guanethidine (15 mg/kg) decreased and even prevented this effect of morphine. Phentolamine pretreatment (10 mg/kg) also significantly inhibited the effect of morphine. Neither DCI nor propranolol influenced this morphine effect. Pretreatment with reserpine, guanethidine or phentolamine reduced the basic pressure threshold needed to elicit peristalsis. The possibility that the decrease of local circulation induced by hypotenison would reduce the local concentration of morphine was rejected because the same doses of guanethidine or phentolamine did not modify the effect of hexamethonium given i.v. in this preparation. All these results support the idea that the effect of morphine on intestinal peristalsis is mediated by a catecholamine acting on alpha-receptors, e.g. norepinephrine.

Animals↗