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Biomedical subjects

J L Devoize

Publications and source records attributed to J L Devoize.

29 records · Page 2Linked to original sources
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↗
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

[Diagnosis of trismus, excluding tetanus and local causes].

The most frequent causes of trismus are tetanus and local lesions. This report discusses other etiologies. Trismus is usually only a secondary sign of a rich clinical picture, but may be of diagnostic value in some cases. Emphasis is placed on the frequency of involvement of neuroleptic intoxication, the early onset of trismus in the malignant hyperthermia syndrome, and on the useful role of trismus in the localization of neurological lesions.

Humans↗
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↗
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

[Benign intracranial hypertension. A clinical, pathophysiological and diagnostic study (author's transl)].

Sixteen unpublished observations of Benign intracranial hypertension were reviewed from a clinical, aetiological and prognostic standpoint. The hypothesis that this affection could be caused by some disturbance of the C.S.F. resorption was assessed using an experimental tests battery allowing the measurement of the main factors involved in C.S.F. resorption. Our patients presented with a pure, solitary state of intra-cranial hypertension, of variable duration, capable of returning. The vital outcome was always favourable, but several severe and protracted cases were marked by a definitive visual damage. The visual risk, often underlined in the literature, requires a careful attention and eventually needs some effective treatment including C.S.F. diversion. A disorder of C.S.F. absorption could be demonstrated in most of our observations and appears to account for the principal features of Benign intracranial hypertension, including the lack of ventricular enlargement. The absorption disorder resulted either from the reversion of the pressure gradient between the C.S.F. and the venous sinuses when a dural sinus was obstructed, - or from an elevation of the resistance to flow when the sinuses were patent, thus suggesting some structural alteration of the arachnoid villi. However, for lack of histological control, such an alteration remains hypothetical, and a primary brain edema probably yield a similar a pathophysiological pattern. Finally, an attempt is made to classify the various aetiological factors encountered in Benign intracranial hypertension according to the previous pathogenic discussion.

Adolescent↗
PubMedDate not supplied

[Dexamethasone test in cluster headache].

Cluster headache and manic depressive illness share in common similarities like: periodic symptomatology, accessibility to lithium therapy, abnormalities in circadian rhythm of cortisol. Though, in contrast to periodic depression, D.S.T. was found normal in 9 patients with cluster headache.

Cluster Headache↗