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J Mardones

Publications and source records attributed to J Mardones.

At least 19 recordsLinked to original sources
PubMed2000

Acute tolerance, alcohol sensitivity and drinking pattern in the F2 generation of UChA and UChB rats.

OBJECTIVE: Studies in mice and rats bred for their behavioral response to ethanol have revealed that there may be a relationship between acute tolerance development, sensitivity to ethanol and alcohol preference. We saw a need to obtain more genetically meaningful correlations between ethanol consumption and acute tolerance to motor impairment or sensitivity to hypothermia induced by ethanol. In the present article, we provide results on acute tolerance, sensitivity to hypothermia and voluntary ethanol consumption in an F2 generation of a cross between inbred UChA (low) and UChB (high) ethanol-consuming rats. METHOD: Naive UChA and UChB rats were tested for acute tolerance development to motor impairment and sensitivity to hypothermia induced by the intraperitoneal administration of a dose of ethanol of 2.3 g/kg body weight. Rats were then offered ad libitum a 10% v/v ethanol solution, distilled water and rat food, and classified according to their drinking scores. Next, one female UChA (low consumer) was mated with one male UChB (high consumer) and one female UChB (high consumer) mated with one male UChA (low consumer). The F2 generation of these inbred rats was used to test acute tolerance, sensitivity and voluntary ethanol consumption. RESULTS: UChB rats developed acute tolerance more rapidly and were less sensitive to the ethanol dose than UChA rats. The F2 generation was designated Hybrid A (HA) for those offspring from the UChA female grandparent and Hybrid B (HB) for the offspring from the UChB female. Results show clearly that there is a relationship between the ability of the rat to acquire acute tolerance to motor impairment, the sensitivity to hypothermia induced by ethanol, and the ethanol preference of the rat. The multiple correlation analysis between the three behaviors showed a significant value in HA rats (r = -0.76, p < .01) and in HB rats (r = -0.83, p < .01). CONCLUSIONS: This study of a cross between UChA and UChB rats showed that the three parameters are related since they clustered together in the F2 generation. This result leads us to speculate that if we could control acute tolerance development in the rats we might also control their voluntary ethanol consumption.

Alcohol Drinking↗
PubMed2000

[Prevalence of anti-hantavirus antibodies in health care personnel in direct contact with patients with hantavirus pulmonary syndrome in Temuco, Chile 1997 to 1999].

BACKGROUND: An outbreak of Hantavirus Cardiopulmonary Syndrome (HVCS) caused by the Andes virus, affected Chile since 1995. Antibodies to Hantavirus in health care workers who had cared patients with HVCS in Coybaique, Argentinean reports and familial clustering of bantaviral illness, raised the possibility of person to person transmission. Familial clustering could occur secondary to a similar exposure to a common infected environment of more than one member of the family. Moreover, the prevalence of antibodies in health care workers in Coyhaique does not differ from the prevalence in general population in that region. AIM: To study the prevalence of antibodies to Hantavirus in health care workers exposed to body fluids of 20 patients. MATERIAL AND METHODS: Among health care workers exposed to patients with HVCS, we registered information about the exposure to patients and to the environment outside the hospital in which they could have been infected. IgG antibodies against Hantavirus were measured by ELISA using two dilutions. RESULTS: Sixty seven workers were studied. Of these, 73% were exposed to respiratory secretions and blood, 21% to blood and 6% to respiratory secretions. Only 6% protected themselves properly, 49% used facial masks and gloves, 25% only facial masks, 7% only gloves and 12% used no protection measures. In none of these workers, Hantavirus antibodies were detected. CONCLUSIONS: These results are supporting evidence against person to person transmission of the Andes virus.

Adult↗
PubMed1999

Differences in ethanol sensitivity and acute tolerance between UChA and UChB rats.

OBJECTIVE: In order to learn more about the genetic factors that determine the different responses to ethanol that contribute to the voluntary consumption of ethanol, this study examines the sensitivity to a nonnarcotic dose of ethanol (2.3 g/kg IP) of rats genetically selected for their low (UChA) and high (UChB) ethanol voluntary consumption. METHOD: Sensitivity was evaluated by studying both ethanol-induced (2.3 g/kg) motor impairment in a modified tilting-plane test and hypothermia. Blood ethanol concentration obtained after the ethanol dose and the correlation between ethanol sensitivity and voluntary ethanol consumption were also studied. RESULTS: Results obtained with both tests revealed that UChB rats were less sensitive to ethanol than UChA ones. The genetic difference in motor impairment appeared not to be the result of different blood ethanol levels. Furthermore, rats of both strains recovered motor activity when blood ethanol was at the highest level, indicating the development of acute tolerance. The acute tolerance appeared to develop in shorter time in UChB than in UChA rats. In contradistinction, time course of hypothermia was significantly related to that of blood ethanol. A significant correlation between motor impairment and ethanol voluntary consumption (p<.001) was obtained. CONCLUSIONS: The difference in motor impairment reported here might be related to differences between the strains in the ability to develop acute tolerance to ethanol. Acute tolerance development appears to be positively correlated to voluntary ethanol consumption by the rat.

Alcohol Drinking↗
PubMed1994

Acetaldehyde metabolism: differences between UChA and UChB rats.

In order to explore the influence of acetaldehyde (AcH) metabolism on the voluntary ethanol intake of genetically low (UChA) and high (UChB) ethanol consumer rats, the AcH disappearance rate (ADR) after incubation with homogenates and subcellular fractions from liver and brain was determined. In addition, the effect of disulfiram pretreatment on AcH metabolism was studied. Male adult rats of both strains were used. ADR was assayed in total homogenates, and in mitochondrial as well as 9000 g supernatant fractions of liver and brain. AcH was measured by gas chromatography. In some experiments, rats were pretreated with disulfiram (300 mg/kg po) 24 hr before the studies. The result showed no strain difference in ADR in homogenates or subcellular fractions of liver from untreated rats, but for disulfiram pretreated rats a significantly lower decrease of ADR in samples from UChB compared to UChA rats was observed. This result is consistent with a lower peak AcH level in UChB compared to UChA rats after a load of ethanol (60 mmole/kg ip). Concerning brain homogenates, a higher ADR was observed in homogenates and crude mitochondrial fractions of UChB than of UChA rats. This difference was not observed when the incubation was performed without adding NAD or in the absence of oxygen. These results provide evidence of strain differences in mitochondrial AcH metabolism, the nature and origin of which deserve further study.

Acetaldehyde↗
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↗
PubMed1981

Genetic differences in tolerance to ethanol: a study in UChA and UChB rats.

The development of tolerance to ethanol was studied in two strains of rats, UChA (low ethanol consumer) and UChB (high ethanol consumer), by the sleeping time test. Marked tolerance (perhaps both metabolic and tissue) appeared in UChA rats, while only a slight tissue tolerance and not a metabolic one appeared in the UChB rats, when they were offered 10% ethanol as the sole fluid during 31 days (p less than 0.001). In UChA, but not in the UChB rats, the chronic treatment with ethanol induced tolerance to pentobarbital as shown by the same test.

Alcoholism↗
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↗