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Copyright of Anaesthesiology & Intensive Medicine / Anesteziologie a Intenzivní Medicína is the property of Czech Medical Association of JE Purkyne and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

A case study of a 74-year-old woman with cardiac myxoma in the left atrium resulting in syncopes is discussed in this article.

The interactions between Ca(2+)-channel blockers (verapamil and gallopamil) and synaptic plasma membranes (SPM) from bovine brain or human lymphocyte and platelet plasma membranes were studied. Changes in binding parameters of [3H]imipramine, [3H]desmethylimipramine and [3H]gallopamil were determined after addition of unlabelled verapamil or imipramine and after addition of phosphatidylserine (PS) (PS-stimulation). Specific binding of [3H]imipramine to SPM was decreased and [3H]desmethylimipramine binding was increased by 1 microM verapamil. [3H]gallopamil binds specifically to SPM as well as to platelet and lymphocyte membranes. [3H]gallopamil binding to SPM or lymphocyte plasma membranes was PS-stimulated in contrast to platelet plasma membranes without PS effect on binding. Imipramine inhibited both [3H]gallopamil binding and PS-stimulated [3H]gallopamil binding to SPM or lymphocyte plasma membranes. Mutual effects of tricyclic antidepressants and Ca(2+)-channel blockers on their binding sites require relatively high drug concentrations. Mechanism of Ca(2+)-channel blockers action in the treatment of depression may be connected rather with changes in signal transduction through serotonin and catecholamine receptor systems than with direct interaction of drugs with binding sites for tricyclic antidepressants.

The author gives a brief account of the action of ATP-ases in the organism. He describes the effect of different substances on the action of these enzymes, whereby special attention is paid to the action of psychopharmaceutical preparations, incl. lithium salts, on the activity of Na+K(+)-ATP-ase. In the experimental part he investigates the activity of ATP-ases in endogenous depressions in our population, the influence of Li+ and electroconvulsions on these enzymes. The results are consistent with data in the literature. Changes in the ATP-ase activities in the course of treatment imply that these enzymes are not genetic markers of depressions. The different effect of therapeutic preparations on the activity of ATP-ases indicates that influencing ATP-ase activity in relation to depressive conditions cannot be considered causal.