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Biomedical subjects

M Feria

Publications and source records attributed to M Feria.

At least 37 records · Page 2Linked to original sources

Stimulation of opioid receptors suppresses penile erectile reflexes and seminal emission in rats.

The effects of several doses of morphine and naloxone, given alone or in combination, on ex copula tests for rat penile erectile responses and seminal emission were studied. Morphine (0.1, 0.5, 1 and 5 mg/kg IP, 30 min before the test) reduced the proportion of animals showing erections in a dose-related fashion. Seminal emission was apparently more sensitive to opioid inhibition than erectile responses, since it was virtually suppressed by all the doses of morphine tested. Naloxone given alone (0.1, 1 and 10 mg/kg IP, 15 min before testing) was largely ineffective on these genital responses although a significant decrease in the display of erection was observed with the lowest dose. Naloxone (1 mg/kg) efficiently antagonized the effects of morphine (1, 5 and 25 mg/kg) on erectile responses and all but the largest dose of the opiate agonist on seminal emission. These results indicate that, in addition to the well-documented effects of opioids on sexual drive, their effects on the genital reflex potential could play a major role in the sexual deficits associated to opiate intake.

Animals↗

Antagonism of the stimulant and depressant effects of ethanol in rats by naloxone.

The action of naloxone (0.5 and 2 mg/kg IP) on the behavioural effects of a low (2 g/kg PO) and a high dose (4 g/kg PO) of ethanol was studied in rats. Ethanol at the low dose increased spontaneous motility, enhancing open-field external ambulations and reducing shuttle-box latency. All these effects were antagonized by naloxone. Ethanol at the high dose produced by hypomotility, decreasing open-field external ambulations and impairing shuttle-box performance. In this case, naloxone also reduced the ethanol effect, but its action was less consistent. Therefore, although mechanisms other than a specific opioid receptor blockade by naloxone must be considered, an involvement of opioid peptides in the effects of ethanol cannot be discounted.

Animals↗

Naloxone-induced increase in blood and brain ethanol concentrations in rats.

Although a reduction in blood ethanol concentration has been proposed to mediate the ethanol antagonist activity of naloxone observed in clinical and experimental situations, an increase in this variable as well as in brain ethanol concentration has been found in rats treated with naloxone (0.5 and 2.0 mg/kg, i.p.) ten min after intragastric administration of ethanol (1 and 2 g/kg). This effect disappeared either when naloxone was administered 50 min after ethanol or when ethanol was given intraperitoneally. On the other hand, naloxone induced a slight but significant slowing in intestinal transit rate. These results suggest that naloxone may facilitate gastrointestinal absorption of ethanol when administered soon after an oral load of this drug. Therefore, mechanisms other than a pharmacokinetic interaction appear to be involved in the antagonist action of naloxone.

Animals↗

Effect of ethanol on neuromuscular function in rats. Its interaction with alcuronium.

The effect of chronic ethanol intake on neuromuscular function has been analyzed by using a rat tibial muscle preparation. The time-course of single twitches, trains-of-four, tetanus and post-tetanic facilitation with and without blockade with alcuronium was evaluated. A decrease in these parameters was observed, being more pronounced in ethanol fed rats during 10 than 30 days. The twitch was the most affected parameter. After recovery of alcuronium blockade, the depressant effects of ethanol were completely reversed. These data suggest that low but sustained ethanol blood levels causes evident alterations of neuromuscular function due, probably, to a postjunctional action.

Alcoholism↗

Effects of dopaminergic agonists and antagonists on the partially contracted, isolated and perfused renal artery of the rat.

The effects of two dopamine agonists, dopamine itself and SKF 38393, alone and in the presence of several dopamine antagonists, have been studied in the partially contracted, isolated and perfused renal artery of the rat. In this preparation, earlier used by other authors in vascular pharmacological experiments, the dopaminergic agents produced clear vasodilator effects which were inhibited by all antagonists used. Due to its low cost and simplicity, such a preparation would be of practical value in testing dopaminergic drugs.

2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-ben↗

Effect of Anesthesia on rat respiration. A study in decerebrated, decerebrated-anesthetized and intact-brain preparations.

The time course of respiratory parameters and blood pressure was studied in decerebrated rats (DR), decerebrated rats treated with a combination of thiopental plus urethane (DAR), and intact brain rats anesthetized with the same combination (IBAR). Moreover, the respiratory sensitivity to a stimulating dose of amphetamine was tested in the three preparations. DR exhibited a spontaneous and steady increase of ventilation which was absent in DAR. A steady increase of ventilation was also observed in IBAR, although of a lesser intensity. Amphetamine induced a clear respiratory stimulation which was decreased by the administration of anesthetics. A tendency to hypotension was seen in all animals. Therefore, the respiratory instability and the decreased pharmacological response observed in the presence of anesthetics are important factors to be considered when interpreting results obtained in this kind of preparations.

Amphetamine↗

Postjunctional Origin of the indirect-like sympathomimetic effect of metanephrine and normetanephrine on blood pressure.

The effects of metanephrine and normetanephrine have been compared with those from equiactive doses of the origin compounds, adrenaline and noradrenaline, on the pressor responses in rat, in order to determine whether their effects are owed, at least partially, to a releasing presynaptic action of the catecholamines in normal animals as well as those pretreated with reserpine, guanethidine and 6-OH-dopamine. Their effects have likewise been studied in isolated perfused renal arteries both in normal and reserpinized rats. None of the adrenolytic agent used were able either to reduce the duration of the hypertensive response or to accelerate tachyphylaxis. Identical results were obtained in renal artery preparations. It is thus concluded that the catecholamines stored in presynaptic endings are not involved in the observed phenomena and it is suggested that they might depend on the high doses required to produce effects equiactive to those of the origin substances.

Animals↗

Ethanol and receptor function.

The effects of ethanol in vitro (21 and 42 mM) and in vitro (10 and 30 days of exposure) on the dose:effect curves for noradrenaline and acetylcholine in isolated auricles and uterus of rats, respectively, have been studied. Likewise, the acetylcholine-atropine interaction was studied in rat uterus under the above-mentioned conditions. Analysis of theoretical curves as well as pD2 and pA2 calculations revealed that ethanol causes changes in the tissue responses to the agents assayed which in turn may be an expression of modification in the receptor function.

Acetylcholine↗

Respiratory effects of amantadine and bromocriptine and their interaction with haloperidol in anesthetized rats.

Amantadine and bromocriptine and caused a dose-related respiratory stimulation in anesthetized rats; in the case of bromocriptine, the highest dose used induced a stimulatory response which was preceded by a decrease in respiratory frequency. The effects were markedly counteracted by the previous administration of haloperidol. It is proposed that the dopaminergic system is involved, at least in part, in the respiratory action of amantadine and bromocriptine.

Amantadine↗