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Biomedical subjects

P Simon

Publications and source records attributed to P Simon.

At least 487 records · Page 27Linked to original sources
PubMed1981

Antagonism of hypothermia and behavioral response to apomorphine: a simple, rapid and discriminating test for screening antidepressants and neuroleptics.

The antagonism of hypothermia induced by two doses of apomorphine (1 to 16 mg/kg) is proposed as an improved screening test for both neuroleptics and antidepressants. Low dose apomorphine-induced hypothermia (1 mg/kg) differentiates sulpiride-like neuroleptics (which better antagonize this effect of apomorphine than other effects such as stereotyped behavior) from haloperidol-like drugs. The latter equally antagonize the two effects of apomorphine. The effects of sulpiride are also distinct from those of chlorpromazine-like drugs which strongly antagonize stereotyped behavior, but not hypothermia induced by apomorphine. Hypothermia induced by a high dose of apomorphine (16 mg/kg) is not antagonized by neuroleptics, but is strongly antagonized by antidepressants (imipramine-like drugs, amineptine, amoxapine, nomifensine, viloxazine) and potential antidepressants (beta-adrenergic stimulants). The use of these two tests rapidly screens both antidepressants and neuroleptics and classifies neuroleptics according to their profile of action on the dopaminergic system.

Animals↗
PubMed1981

Effects of drugs affecting the noradrenergic system on convulsions in the quaking mouse.

Handling-induced convulsions in the quaking mouse can be blocked by: phenobarbital, pentobarbital or phenytoin; postsynaptic alpha-adrenoceptor agonists (noradrenaline, phenylephrine, CRL 40028); presynaptic alpha-adrenoceptor blockers (yohimbine, mianserine); catecholamine liberating agent (amphetamine); noradrenaline reuptake inhibitors (cocaine, imipramine, desipramine). Moreover, the protective effect of yohimbine was antagonized by clonidine, prazosin or alpha-methylparatyrosine, and the protective effect of CRL 40028 was antagonized by prazosin but not by alpha-methyltyrosine. Drugs acting by other mechanisms (pilocarpine, atropine, trihexyphenidyl, (--)-5-HTP, methysergide, pimozide, clonidine, alpha-methyl DOPA, prazosin, isoprenaline, salbutamol) did not protect against convulsions. A slight protection was obtained with high doses of apomorphine and also with (+/-)-propranolol. This effect is probably not related to blockade of beta-adrenoceptors because the same effect was obtained with (+)propranolol. In young quaking mice, where susceptibility to convulsions is low, both postsynaptic alpha-adrenoceptor blockers and presynaptic alpha-adrenoceptor antagonist lowered the convulsive threshold. Thus, this seems to constitute an interesting model for the in vivo study of substances which affect the central alpha-adrenoceptors either pre- or postsynaptically.

Animals↗
PubMed1981

Triazolam compared with nitrazepam and with oxazepam in insomnia: two double-blind, crossover studies analyzed sequentially.

1 In two double-blind, crossover studies, general practitioners compared the hypnotic activity of triazolam 0.50 mg with that of nitrazepam 5 mg or oxazepam 50 mg in outpatient insomnias. 2 The patient's preferences served as the main criterion, and were processed by sequential analysis. 3 More patients (P less than 0.05) preferred triazolam to nitrazepam (triazolam 28; nitrazepam 11; no preference 9). 4 The numbers of patients who preferred triazolam or oxazepam did not differ significantly. 5 Triazolam and oxazepam affected sleep parameters similarly except for onset of sleep and feeling in the morning, for which triazolam seemed to be superior to oxazepam.

Adolescent↗
PubMed1981

Reduction of Vanadate by ascorbic acid and noradrenaline in synaptosomes.

The effect of ascorbic acid and noradrenaline on the inhibition of synaptosomal membrane ATPase by vanadate has been studied. Ascorbic acid (2 x 10(-3) M) and noradrenaline (10(-4) M) partly reversed the inhibition by vanadate (10(-6) M); however, when both were administered together the inhibition was completely eliminated. Using electron spin resonance (ESR) spectroscopy, we detected that ascorbic acid (10(-3) M) caused a 42% of reduction of vanadate (10(-4) M). Noradrenaline (10(-4) M) alone also reduced vanadate (10(-4) M) partially. When ascorbic acid and noradrenaline were present together all the vanadate was reduced to vanadyl. The concentration of ascorbic acid present in the brain under physiological conditions is identical to that found effective in our experiments. We suggest that ascorbic acid may protect the ATPase, at least in part, from inhibition by vanadate as a consequence of reducing vanadate to vanadyl. In those tissues where noradrenaline is also present a complete reduction of endogenous vanadium can be presumed.

Animals↗
PubMed1981

Beta-adrenergic stimulation and antidepressant activity.

The results presented here, together with the literature data, support the noradrenergic hypothesis of depressive states, and especially the involvement of beta-adrenergic receptors: --In animals, beta stimulants have the same spectrum of activity as other antidepressants. --These effects of both classical antidepressants and beta-adrenergic stimulants are antagonized by beta blockers. --Chronic administration of antidepressants results in a decrease of beta receptors. --Salbutamol, a beta-adrenergic stimulant had, in depressed patients, a clear and rapid antidepressant effect.

Adrenergic beta-Agonists↗
PubMed1981

[The new versus the old antidepressant drugs: a comparative study of their psychopharmacological profiles (author's transl)].

We studied 13 known or potential antidepressants, choosen in different pharmacological classes: desipramine, imipramine, nialamide, dexamphetamine, AHR 1118, amineptine, iprindole, mianserine, nomifensine, salbutamol, TRH viloxazine, zimelidine. Each of these compounds was studied on 8 psychopharmacological tests: motor activity, reserpine induced hypothermia, reserpine induced ptosis, oxotremorine induced hypothermia, oxotremorine induced tremors, high doses apomorphine induced hypothermia, potentiation of toxic effects of yohimbine, behavioural despair. Clinical active compounds are efficient on yohimbine test and at least on one model of hypothermia; with a few exceptions, easy to explain, substances with a clearly demonstrated antidepressant activity in human have some common effects; these common effects can be used to predict, from animal experiments, an antidepressant effect in man.

Animals↗
PubMed1981

[Iron-overload in patients on maintenance hemodialysis: diagnostic criteria, indications and treatment by desferrioxamine (author's transl)].

33 patients with chronic renal failure were divided into two groups. Group I consisted of 8 non-dialysed patients without any clinical or biochemical sign of liver disturbance nor any iron supplementation. Group II consisted of 25 maintenance hemodialysis (MHD) patients treated from 2 to 13 years. 19 subjects had chronic B hepatitis. Total exogenous iron load parenteral iron and/or blood transfusions) was calculated. Body iron overload (hemosiderosis) was assessed by liver iron concentration (LIC) in needle biopsy specimens according to Barry's method (less than 200 microgram/100 mg dry weight) and serum ferritin levels (less than 360 ng/ml). 4 patients whose serum ferritin was increased with or without hepatic fibrosis and with or without any organ dysfunction due to hemochromatosis received i.v. infusions of desferrioxamine in doses of 2 g at each dialysis. Serum ferritin levels were correlated with LIC (p less than 0.001) and iron load (p less than 0.001). Hemosiderosis was noted in 16 MHD patients (group II) and correlated with iron load. Hemochromatosis was noted in 4 patients (group II). 4 hemodialysed patients with iron overload were treated by desferrioxamine from 6 to 18 months. During this therapy, body iron stores fell and organ dysfunction (heart failure, hepatic cytolysis, anaemia, diabetes mellitus improved. Long-term chelation therapy by desferrioxamine was effective and the chelated iron was readily removed by dialysis. These data show the importance of precise evaluation of iron stores in MHD patients.

Adult↗
PubMed1980

Improvement of anaemia in haemodialysed patients after viral or toxic hepatic cytolysis.

Thirty patients receiving haemodialysis, including two who had undergone bilateral nephrectomy, showed significant increases (p less than 0.001) in packed cell volume, haemoglobin concentration, and reticulocyte count during an episode of viral or toxic liver cytolysis. In 19 cases the episode lasted a mean of 5.0 +/- SD 2.9 months and was accompanied by improved haematological values for a mean of 12.0 +/- 6.0 weeks. Of the remaining patients, in whom the episode lasted a mean of 8.0 +/- 3.5 months (p less than 0.02), seven showed continued improvement a mean of 30.0 +/- 16.0 weeks after cytolysis. In eight patients in this group there was an apparent correlation between persistently increased haemoglobin concentrations and biopsy evidence of chronic hepatitis. The findings suggest that the reduction in anaemia resulted from enhanced red-cell production mediated by secretion of erythropoietin from regenerating liver cells. If confirmed this might have important implications for the treatment of anaemia in chronic renal insufficiency.

Adolescent↗
PubMed1980

Oxolinic acid and diazepam: their reciprocal antagonism in rodents.

The stimulant effects of oxolinic acid were investigated in rats and mice. This drug, given orally, consistantly induced, in doses ranging from 16 to 256 mg.kg-1, locomotor stimulation and stereotyped behavior. These effects were antagonized by pimozide (1 mg.kg-1), alpha-methyltyrosine (64 mg.kg-1) or reserpine (4 mg.kg-1, 24 h before testing) pretreatment, suggesting a facilitatory role of oxolinic acid on catecholaminergic processes. Diazepam (4-16 mg.kg-1) reduced the stimulant effects induced by oxolinic acid but not those induced by amphetamine; oxolinic acid (8 mg.kg-1) markedly reduced the antipunishment effect elicited in rats by diazepam (2 mg.kg-1). Since benzodiazepines have been reported to enhance GABA functioning, these data suggest that oxolinic acid may impair GABA transmission. However, neither muscimol (0.5-1 mg.kg-1) or gamma-acetylenic-GABA (16-64 mg.kg-1) selectively reduced the stimulant effects elicited by oxolinic acid. Therefore, the possible facilitation exerted by this drug on catecholaminergic systems may not derive from the release of an inhibitory GABAergic control.

Animals↗