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Biomedical subjects

L Baran

Publications and source records attributed to L Baran.

At least 37 records · Page 2Linked to original sources
PubMed1980

[Giant aneurysm of the internal carotid artery, stimulating parasellar tumor].

The authors report a case of a giant aneurysm of the internal carotid artery filling from the left internal carotid artery below the site of branching-off of the posterior communicating artery. The initial neurological, and ophthalmological signs and plain films of the skull suggested presence of an Erdheim's tumour. It is worth stressing that the onset of the clinical manifestations was at the age of 15 years, particularly in the form of progressing binasal hemianopsia with sparing of the lower temporal quadrant. The efficiency of the cerebral circulation was tested using Mathas' test, electroencephalography, ophthalmodynamometry and angiography. It was decided to ligate the left carotid artery although Mathas' test during angiography was not as positive. The boy tolerated the operation well. Ophthalmological examination demonstrated after 18 months normal visual fields and normal visual acuity. Further follow-up during 8 years demonstrated normal psychosomatic development of the boy.

Adolescent↗
PubMed1979

The central action of pizotifen.

The central action of the potential antidepressant drug pizotifen (Sandomigran) was studied in mice, rats and rabbits. Pizotifen in doses up to 10 mg/kg i.p. was ineffective in classic tests for antidepressant activity. It neither antagonized the effects of reserpine in rats (hypothermia, ptosis) nor potentiated the effects of amphetamine (in mice and rats), nialamide or L-dopa (in mice) on locomotor activity. However, its antidepressant activitiy was found in the 'despair test' in rats. On the other hand, pizotifen inhibited the head twitch reaction induced by L-5-hydroxytryptophan in mice (ED50 = 0.009 mg/kg, i.p.) and by 5-methoxytryptamine (+ tranylcypromine) in rats (ED50 = 0.45 mg/kg, i.p.). It also antagonized tryptamine-induced clonic convulsions of fore-paws in rats (ED50 = 0.35 mg/kg, i.p.), and in doses of 5--10 mg/kg s.c. inhibited hyperthermia produced by LSD in rabbits. Finally, pizotifen (0.1--0.3 mg/kg, i.v.) inhibited or abolished LSD- or quipazine-induced stimulation of the hind limb flexor reflex of spinal rats; the above effect was not due to noradrenolytic action of the drug. These results suggest that pizotifen strongly blocks the central postsynaptic serotonin receptors.

Amphetamine↗
PubMed1978

The central antiserotonergic action of mianserin.

The central antiserotonergic action of mianserin (MS) was tested in mice, rats, and rabbits. MS, like cyproheptadine, to which it was compared, inhibits the head-twitch response to 5-hydroxytryptophan in mice and rats without affecting the pinna reflex. MS does not change the flexor reflex of the hind limb of the spinal rat; it antagonizes its stimulation induced by fenfluramine, LSD, and quipazine, but not that induced by clonidine. The hyperthermia in rabbits caused by the serotonergic stimulants cited above is also antagonized by pretreatment with MS. Unlike cyproheptadine, MS is not active in the oxotremorine test. The results indicate that at low doses MS is a central serotonergic-receptor blocker.

Animals↗
PubMed1976

The effects of serotonergic and antiserotonergic drugs on the flexor reflex of spinal rat: a proposed model to evaluate the action on the central serotonin receptor.

The effects of serotonergic and antiserotonergic drugs on the hind limb flexor reflex (measured as a contraction of musculus tibialis anterior or as a flexion of the paw) in the spinal rat was studied. All serotonergic drugs used (L-5-hydroxytryptophan, L-tryptophan, LSD, fenfluramine, p-chloroamphetamine) stimulate the flexor reflex. Serotonin receptor blockers (cyproheptadine, WA-335, methergoline), which given alone are inactive, inhibit the stimulation induced by serotonergic drugs but do not influence that one caused by noradrenergic agents (amphetamine, clonidine). Both types of stimulation (serotonergic and noradrenergic) are antagonized by noradrenaline receptor blockers (phenoxybenzamine, clozapine). The antiserotonergic action of serotonin antagonists used was confirmed on the basis of the antagonism to the head twitches induced by L-5-hydroxytryptophan. The flexor reflex in the spinal rat may be a good model to evaluate the effect on the central (spinal cord) serotonin receptor and to differantiat this effect from that on the noradrenaline system.

5-Hydroxytryptophan↗
PubMed1976

Influence of WA-335, a factor which blocks serotonin receptors, on neuroleptic-induced catalepsy.

In a previous study, anticataleptic action of cyproheptadine was reported. The present investigation deals with the influence of WA-335 (9,10-dihydro-10-(1-methyl-4-piperidylidene)-9-anthrol), another antagonist of serotonin, on catalepsy induced in rats with spiroperidol, pimozide, fluphenazine and reserpine. WA-335 antagonized catalepsy induced by these neuroleptics (the effect on reserpine-induced catalepsy was weakest). Joint administration of WA-335 and L-DOPA with an inhibitor of peripheral decarboxylase, or WA-335 and amantadine produced a stronger antagonistic effect (spiroperidol catalepsy) than either of these substances separately. WA-335 did not prevent catalepsy induced with physostigmine.

Amantadine↗
PubMed1976

The action of compound WA-335 on the central nervous system.

Compound WA-335 (9,10-dihydro-10-(-1-methyl-4-piperidylidene)9-anthrol) was studied with regard to its antidepressant and central antiserotonin action in mice and rats. WA-335 depresses reserpine-induced hypothermia, particularly in mice, but does not affect ptosis induced with this neuroleptic. The compound diminishes spontaneous motility in mice and rats, including mice stimulated with amphetamine. WA-335 acts synergistically with amphetamine in which it potentiates stereotyping and enhances motility. The compound has no influence on the action of L-DOPA and does not alter hypothermia or increase motility induced with this amino acid. WA-335 does not affect the drop in body temperature or stereotype induced with apomorphine. In mice, WA-335 inhibits motility elicited with L-5-hydroxytryptophan, and in rats as well as mice prevents occurrence of head-twitches due to activation of serotonin neurons. The compound has no effect on the righting reflex abolished with fenfluramine in frogs, and given together with reserpine slightly counteracts abolition of this reflex. WA-335 raises the level of serotonin in the brains of rats, and lowers the level of 5-hydroxyindoleacetic acid. In addition, WA-335 exhibits cholinolytic activity and abolishes the symptoms elicited with oxotremorin in mice and rats.

Amphetamine↗
PubMed1975

The effect of 5-hydroxytrytamine synthesis inhibitors on neuroleptic-induced catalepsy in rats.

The influence of factors which inhibit 5-hydoxytryptamine (5-HT) synthesis, i.e. p-chlorophenylalanine (PCPA) and p-chloroamphetamine (PCA), on cataleptic action of the neuroleptics: spiroperiodol, pimozide, reserpine and fluphenazine was studied. PCPA showed weak anticataleptic activity in reserpine-induced catalepsy but had no effect on catalepsy induced by spiroperidol or fluphenazine. PCPA also tended to depress the cataleptic effect of pimozide, but the results were not statistically significant. PCA had no influence on catalepsy induced by neuroleptics from the group of butyrophenones, potentiated the cataleptic action of reserpine in the dose of 5 mg/kg, and suppressed catalepsy induced by reserpine in the dose of 10 mg/kg. The results suggest that under conditions of the inhibition of the inhibition of 5-HT synthesis the cataleptic action of some neuroleptics may be slightly modified.

Amphetamines↗