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Biomedical subjects

A Eschalier

Publications and source records attributed to A Eschalier.

At least 127 records · Page 7Linked to original sources
PubMed1986

Acute hemodynamic effects of an antitumoral agent: elliptinium. Involvement of histamine release.

This work reports a study of cardiovascular effects of elliptinium, a recently-acquired antitumoral agent, acutely administered i.v. in the dog. Its hemodynamic effects (10 parameters) are detailed, and their mechanism of action is investigated by antagonist administration and determination of blood and plasma histamine levels. Elliptinium induces vasodilation and tachycardia. The former is mainly due to histamine release, and a brief and slight release of prostaglandins; the latter is due to a reflex to hypotension and release of catecholamines. These results agree with others using various compounds of the ellipticine family and anthracycline antitumoral agents. They suggest treatment to prevent anaphylactoid side effects observed with this drug in man and they raise the question of the usefulness, in antitumoral agent, of histamine releasing properties.

Alkaloids↗
PubMed1985

Chemical structure and hemodynamic effects of two new pyridazinone derivatives.

Two new pyridazinone derivatives were selected among two series and assayed for their hemodynamic effects. Their synthesis is described and their chemical structure confirmed by I.R. and N.M.R. data. The 5-arylhydroxymethyl-3-pyridazinone did not induce any significant hemodynamic changes. However, the 5-dichlorobenzylidene-3-pyridazinone, intravenously injected, was active in anesthetized dogs. Moderate doses induced modifications in the heart rate, left ventricular dP/dt max and femoral blood flow and resistance.

Animals↗
PubMed1985

Cardiac and vascular effects of elliptinium in guinea pigs. Involvement of a histaminergic mechanism.

This work reports a study of the effects of elliptinium on heart rate, arterial blood pressure and capillary permeability in guinea-pigs. The variations in capillary permeability are determined by spectrophotometric assay of skin Evans blue. Elliptinium induces dose-independent tachycardia and dose-related hypotension. For the highest dose (6 mg/kg), elliptinium induces lethal collapse . Elliptinium increases capillary permeability and this effect, particularly marked at 1 mg, i.d., is partially antagonized by mepyramine-cimetidine association. These results are discussed in comparison with those obtained with elliptinium on other parameters, with histamine and with different antitumoral agents. The increase in capillary permeability raises the question of its relevance to the anticancer activity of elliptinium.

Alkaloids↗
PubMed1984

[Clinical and pharmacologic aspects of the analgesic effect of tricyclic antidepressants].

Although tricyclic antidepressants have now been used for more than 20 years in the treatment of chronic pain, controlled studies of their effectiveness are quite recent. The best results are obtained in pain due to peripheral nerve lesions, and high doses are recommended. In contrast with the slow onset of their effect on depression, these drugs promptly relieve pain, which suggests two different mechanisms of action. The analgesic mechanism is unknown; some data indicate that serotonin is involved but an action on the adrenergic system cannot be ruled out. The arguments supporting the recent endorphin hypothesis are reviewed, ad a possible relationship between tricyclic antidepressants and endorphins is envisaged.

Analgesics↗
PubMed1984

Bronchopulmonary effects of elliptinium in anesthetized dogs.

The bronchoconstrictor effect of elliptinium already demonstrated in the guinea-pig is shown in the dog. It is less intense and its onset is prompter. Successive administration of identical doses of elliptinium attenuates the bronchospasm induced, suggesting tachyphylaxis. The previously described indirect bronchoconstrictor effect involving endogenous mediators seems also to be active in these circumstances.

Alkaloids↗
PubMed1984

Influence of naloxone on antidepressant drug effects in the forced swimming test in mice.

The influence of naloxone on the effects of several antidepressant drugs, atropine and caffeine was studied in the forced swimming test in mice. Naloxone itself has no effect in this test, but significantly reduces that of two tricyclic antidepressants, clomipramine (20 and 30 mg/kg) and desipramine (20 and 30 mg/kg). Except for clorgyline at the high dose of 60 mg/kg, no significant reduction of activity by naloxone was observed with other antidepressants (pargyline, nomifensine and mianserin), nor with caffeine and atropine. These results are discussed in terms of the pharmacological characteristics of each drug and of the test used. No straightforward interaction between cholinergic or monoaminergic and endorphinic systems is evident. Possible action at opiate receptor sites is discussed.

Animals↗
PubMed1984

Effect of a reversible and selective MAO-A inhibitor (cimoxatone) on diurnal variation in plasma prolactin level in man.

Prolactin (PRL) secretion is stimulated by serotonin (5-HT) and inhibited by dopamine (DA). 5-HT is generally recognized as a substrate for type A monoamine oxidase (MAO), whereas DA is considered as a substrate for either A or B, or both forms of MAO, depending on the species and tissues used. The effect of cimoxatone, a reversible, selective MAO-A inhibitor, on diurnal variation in plasma PRL level was investigated in healthy adults after a single 40 mg oral dose, as an indirect approach to investigating whether DA is preferentially a substrate for Type A or B MAO in man. The circadian rhythm in PRL, stress conditions and diet were taken into account in the present study, which was placebo-controlled. There was a slight but significant reduction in circulating PRL in the six subjects, which persisted for at least 9 h after cimoxatone. However, the duration of the decrease in plasma PRL was shorter than the inhibition of MAO-A. The results are not inconsistent with the presence of both forms of MAO in the human hypothalamus and with DA as a substrate for both forms in this region, if it is assumed that the hypothalamic concentrations of the drug during the period 0-9 hours was sufficiently high to inhibit DA deamination by both forms of MAO.

Adult↗
PubMed1984

Is there any relationship between antinociception, doses and plasma levels of clomipramine during subchronic treatment in rats?

The antinociceptive effects and the plasma levels (evaluated by high liquid pressure chromatography) of clomipramine during a subchronic (5 days) treatment were studied in rats using the Nilsen's test. Clomipramine (10, 20, 30 and 40 mg/kg administered by mouth) showed a clear dose-dependent analgesic effect. The study of the partial correlation coefficients did not found a relationship between plasma levels and antinociception under our experimental conditions. These results suggest that regular monitoring of plasma levels of clomipramine appears to be useless in the treatment of patients with chronic pain.

Analgesics↗
PubMed1983

Morphine pretreatment reduces clomipramine effect in mouse forced-swimming test.

It had previously been shown that naloxone inhibits the effect of clomipramine both in a pain test in the forced-swimming test in mice which is proposed as an antidepressant study model. Evidence is reported of a decrease in activity of clomipramine in the forced-swimming test in mice after morphine pretreatment. The hypothesis of an interaction with mu-opiate receptors is considered.

Animals↗
PubMed1983

Activities of five antidepressants in a behavioral pain test in rats.

Various clinical and experimental reports indicate that antidepressant drugs can have analgesic properties. The authors tested successively the anti-nociceptive activity of desipramine, clomipramine, maprotiline, viloxazine and nomifensine on the acute experimental pain model designed by Charpentier. At 25 mg/kg, desipramine showed a marked antalgic action. Clomipramine and maprotiline had a similar though much weaker action. On the other hand, nomifensine and viloxazine did not reduce pain perception; their effects on the parameters studied were variable. The usefulness of the test itself is discussed and suggestions are made regarding the relations between the analgesic potency of the drugs and the main neurotransmitter system they are assumed to act on.

Analgesia↗
PubMed1983

A comparison of the effects of vitamin B12 and aspirin in three experimental pain models in rats and mice.

The effects of vitamin B12 are compared to those of aspirin and 0.9% saline in three different experimental pain models in rats and mice; an electric shock test, the hot-plate test, and the phenylbenzoquinone writhing test. Neither cyanocobalamin nor hydroxocobalamin showed any antinociceptive activity in any of the three tests at any of the doses used, whether the drug was administered as a single injection or as a series of daily injections lasting 7 days. These results run counter to those of clinical trials in man, though close scrutiny of the experimental procedures used in these trials often reveals a lack of rigor which casts doubts on their validity. This consideration, together with the negative findings reported here, suggests that the clinical use of vitamin B12 as an analgesic may be inappropriate.

Analgesics↗
PubMed1982

Naloxone inhibits clomipramine in mouse forced swimming test.

Naloxone inhibited the effect of clomipramine on duration of immobility of mice in the forced swimming test. This test is proposed as an antidepressant study model. It had previously been shown that naloxone inhibited the analgesic effect of the antidepressant clomipramine. Several hypotheses are considered for the mechanism of the naloxone-clomipramine antagonism.

Animals↗
PubMed1982

Comparison of the effects of propranolol, pindolol, oxprenolol and acebutolol on atrioventricular conduction in unanaesthetized dogs.

1 Atrio-ventricular conduction (AVC) in the unanaesthetized dog (17 animals) was studied using atrial pacing at progressively increasing frequencies applied via electrodes implanted in the right atrium. In animals habituated to the experimental conditions, beta-adrenoceptor blocking drugs devoid of intrinsic sympathomimetic activity (ISA) modified neither heart-rate (HR) nor AVC, though 4 mg/kg i.v. propranolol transiently raised HR and facilitated AVC. Due to their ISA, pindolol and oxprenolol raised HR and facilitated AVC at high doses. 2 Thus, when not under anaesthesia, the resting dog, in contrast to man, possesses no tonic adrenergic influence which might be suppressed by beta-adrenoceptor blockings drugs. 3 After atropine or pentobarbitone, which considerably increased HR, beta-adrenoceptor blocking effects became clearly visible, and the hitherto reported depressant effects on HR and AVC were observed. However, the ISA of oxprenolol, and especially of pindolol, can partly or completely mask their beta-adrenoceptor blocking action at high doses under these experimental conditions.

Acebutolol↗
PubMed1981

Influence of naloxone and methysergide on the analgesic effect of clomipramine in rats.

The effects of the tricyclic antidepressant clomipramine were studied in two analgesic tests in rats: (1) vocalization threshold response; and (2) scored behavioral response to electric shock to the tail. Clomipramine (20-50 mg/kg i.p.) produced analgesia, decreasing behavioral response scores and increasing vocalization threshold. Morphine also reduced the response scores in the second test. Naloxone (0.8 mg/kg i.p) or methysergide (20 mg/kg i.p.) (no effect when given alone) abolished the analgesic effect of clomipramine as evaluated by vocalization threshold response. Naloxone alone (0.6 or 2 mg/kg i.p.) increased the behavioral response at 20 and 30 V but did not modify the score at 40 V. Naloxone reduced the analgesic effect of clomipramine or morphine in the behavioral test. These results suggest that the analgesic effect of clomipramine could involve both serotonergic and endorphin central systems.

Analgesics↗
PubMed1981

Histamine-releasing properties of hydroxy-9-methyl-2-ellipticinium acetate.

Previous work on Hydroxy-9-methyl-2-ellipticinium acetate indicated a bronchoconstrictor activity which could be partially offset by antagonists of the H1 histamine receptors, and the absence of any direct effect on smooth muscle. OH-9-CH3-2-E at concentrations of 10 micrograms/ml and 500 micrograms/ml produced a moderate and a variable release of histamine when placed in contract with whole human blood and lung fragments, respectively. In addition, at a dose of 3 mg/kg in the guinea pig, pulmonary airway resistance was raised and the blood histamine level lowered. A significant correlation was found between these two effects. These results demonstrate that OH-9-CH3-2-E possesses a histamine-releasing potency which is partly responsible for its bronchial effects, implying that precautions may have to be taken when it is used as a therapeutic agent in sensitive subjects. However, the moderate intensity of this potency has not so far precluded therapeutic use of the preparation.

Airway Resistance↗
PubMedDate not supplied

Plasma and brain pharmacokinetics of amitriptyline and its demethylated and hydroxylated metabolites after acute intraperitoneal injection in mice.

The fate of amitriptyline (AMI) and its demethylated and hydroxylated metabolites was studied in Swiss CD1 mice, after acute intraperitoneal injection of AMI (20 mg/kg). Levels of each compound were determined to establish pharmacokinetic parameters in plasma and brain. Absorption and elimination of AMI were rapid (tmax = 0.37 h and 0.42 h, and t1/2 = 3.2 h and 3.6 h in plasma and brain, respectively). In plasma, 10-OH-nortriptyline was the main metabolite (46% of AUC) and 10-OH-amitriptyline reached significant levels but only during the first hour. In brain, AMI (43% of total AUC), nortriptyline (NOR) (29%) and demethylnortriptyline (DM-NOR) (11%) were the most abundant compounds, possibly through high blood-brain barrier transfer and/or marked intracerebral demethylation. Brain OH-metabolite levels were much lower. Knowledge of kinetic parameters and metabolism of AMI can help in the evaluation of pharmacological activity.

Amitriptyline↗