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At least 1,621 records · Page 90Linked to original sources
PubMed1980

[Pathogenetic therapy of cobalt-induced cardiomyopathies].

The pathogenesis of damage to the heart muscle caused by exposure to the effect of cobalt compounds is demonstrated. Agents with various mechanisms of action were tested in the experiment. The most effective pharmacological agents (beta-adrenergic blocking agents, anabolic steroids) are recommended for testing in the clinic. A positive effect was registered in the treatment of cobalt cardiomyopathy in the clinic. The mechanisms of the favourable effect of beta-adrenergic blocking agents and anabolic steroids are discussed.

Adrenergic beta-Antagonists↗
PubMed1982

Neural serotonin stimulates chloride transport in the rabbit corneal epithelium.

Evidence is presented that serotonin acts as a neurotransmitter in the cornea of the adult rabbit. Serotonin was localized to granules in a sparse population of subepithelial corneal nerves by an electron microscopic histochemical procedure. Significant endogenous levels of serotonin and its principal metabolite, 5-hydroxyindoleacetic acid, were detected in the central cornea by a fluorometric assay. Exogenous serotonin stimulated ion transport by corneal epithelium. This effect was potentiated by monoamine oxidase inhibition and was unaffected by an alpha-adrenergic receptor antagonist. Serotonin-stimulated ion transport was inhibited by the specific antagonist, methysergide, and by the replacement of Cl- with an impermeable anion. In tracer experiments, the serotonin-stimulated ion transport was shown to be caused by increased epithelial Cl- secretion. The serotonin response was partially inhibited by the beta-adrenergic antagonist, timolol. In a companion article, assay of corneal cyclic AMP showed stimulation of cyclic AMP synthesis by serotonin, inhibition by the specific antagonist, lysergic acid diethylamide, and potentiation by monoamine oxidase inhibition. We postulate that specific serotonergic receptors are present in the corneal epithelium and that activation of these receptors by serotonin released from serotonergic neurons increases the level of cyclic AMP, which stimulates active Cl- secretion by the corneal epithelium.

Animals↗
PubMed1975

[Borderline between antiepileptic and psychopharmacological drugs (author's transl)].

From the chemical and pharmalogical point of view it is impossible to separate strictly between antiepileptic and psychopharmalogical drugs. Inspite of that and several clinical overlappings it is possible and helpful finding differences between the two groups of drugs. Basing on the indication we try to demonstrate the use of these drug-groups. 1. Antiepileptic drugs in behaviour disorders. A. In spite of various publications we recommend carefullness and restriction. B. Only in case of behaviour disorders due to epileptic origin antiepileptic therapy is indicated. 2. Psychopharmalogical drugs in epilepsies A. The frequency of seizures may be reduced B. Psychical disorders connected with seizures may be influnced.

Amitriptyline↗
PubMed1978

[Effect of echinopsin and adepren on motor activity in rats].

We have studied the influence of synthesized in NIHFI psychotropic drugs echinopsin and adepren for their locomotor activity on white rats in open field and staircase. Comparative parallel experiments were carried out with psychostimulants and antidepressive drugs utilized in therapeutic practice. We found that echinopsin in low doses increases the locomotor activity and in large doses decreases. Its action in open-field and staircase is different from the effect of amphetamine and coffeine which is confirmed by clinical evidence. Adepren decreases the locomotor activity in single application as a result of decreasing of brain noradrenaline which is similar to the effect of MAOI drugs.

Aminoquinolines↗
PubMed1980

Monoamine oxidase inhibitors and serotonin uptake inhibitors: differential effects on [3H]serotonin binding sites in rat brain.

Rats were administered either monoamine oxidase inhibitors or serotonin uptake inhibitors for either 1, 4 or 16 days. The binding of [3H]serotonin to brain homogenates and the concentration of serotonin in brain was measured at these times. Treatment with inhibitors of serotonin uptake did not change the specific binding of [3H]serotonin in either cerebral cortex or hippocampus, nor did it produce any consistent alterations in the concentration of serotonin in the cerebral cortex. In contrast, monoamine oxidase inhibitors capable of inhibiting A-type monoamine oxidase significantly decreased [3H]serotonin binding after both 4 and 16 days of treatment; serotonin concentrations were significantly elevated at all time intervals. Inhibitors of B-type monoamine oxidase had no effect on either [3H]serotonin binding or serotonin concentrations in cerebral cortex. The reduction in labeled serotonin binding caused by monoamine oxidase inhibitors is due to a decrease in the maximum number of specific binding sites with no change in the affinity of the binding sites for labeled serotonin.

Amitriptyline↗
PubMed1980

A system of atypical catecholamine-containing nerve fibres in the rat iris present after total superior cervical ganglionectomy.

A system of hitherto unknown weakly fluorescent fibres was detected in the rat iris by Falck-Hillarp fluorescence histochemistry after superior cervical ganglionectomy. These long smooth winding (SW)-fibres had a scarce and unusual distribution, forming loops and meandering for long distances with limited branching. Pharmacological tests suggest that they store a catecholamine but differ from adrenergic nerves in lacking an efficient uptake mechanism for amines. SW-fibres reached all parts of the iris and gave rise to few scattered extremely faint green fluorescent, limited plexuses of irregularly bulgy fibres. Suggestions as to the cellular origin of the SW-fibres include the ciliary ganglion and the central nervous system.

Animals↗