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PubMed1975

[Problems in the use of cardiac glycosides in ischemic heart disease].

With the help of instances from literature and own experimental and clinical experiences is described that a schematic digitalisation in ischaemic heart diseases is not worth being advocated scientifically. Heart glycosides are indicated especially then, when a heart insufficiency stands in the foreground. In the acute phase of infarction, without manifest heart insufficiency, however, in individual cases they can deteriorate the myocardial oxygen balance and thus the clinical course. In myocardial infarction with severe heart insufficiency up to the cardiogenic shock all therapeutic possibilities should be utilized; to this belongs also the application of glycosides. As a rule in cardiogenic shock after myocardial infarction glycosides have no sufficient measurable influence on haemodynamics. Heart glycosides together with an individually adapted kinetotherapy are of importance for the metaphylaxis in patients with infarction.

Cardiac Glycosides↗
PubMed1988

Interactions of cardiac glycosides with cells and membranes. IV. Effects of ouabain and bumetanide on 86Rb+ influx in cultured cardiac myocytes from neonatal rats.

Ouabain at nanomolar concentrations stimulates total Rb+ influx by 20 +/- 2% in monolayer cultures of myocytes which were either in physiologic ionic steady-state conditions ('control') or 'loaded with Na+' following exposure to K+-free medium. The ouabain-stimulated Rb+ influx was completely abolished by 0.1 mM bumetanide both in 'control' and in 'Na+-loaded' myocytes. Thus, addition of nanomolar concentrations of ouabain to myocytes markedly stimulate the bumetanide-sensitive Rb+ influx. This influx was increased up to 3- and 4-fold in 'control' and 'Na+-loaded' myocytes, respectively. Ouabain at nanomolar concentrations had no significant effect on the component of 86Rb+ influx which is inhibited by millimolar concentrations of ouabain (the so called 'ouabain-sensitive' or 'pump-mediated' Rb+ influx) in 'control' and 'Na+-loaded' cells. It is proposed that the increased rates of bumetanide-sensitive Rb+ influx are accompanied by an increased bumetanide-sensitive Na+ influx through the Na+/K+ cotransporter and thus to a transient increase in intracellular Na+ concentrations [Na+]i. The increase in [Na+]i, subsequently causes a transient elevation in [Ca2+]i via the Na+/Ca2+ exchanger and may be involved in the regulation of cardiac cells' contractility.

Animals↗