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Protective effect of creatinol O-phosphate (COP) on ventricular fibrillation and death induced by intravenous CaCl2 in mice.

The activity of N-methyl-N-(beta-hydroxyethyl)guanidine O-phosphate (creatinol O-phosphate, COP) on the acute toxicity of CaCl2 in mice was studied. The results obtained in the present investigation show that COP administered i.v. is able to antagonize, in a dose-dependent way, the lethal ventricular fibrillation provoked by CaCl2 in unanesthetized mice. Prenalamine and cinnarizine, two calcium antagonistic compounds, proved to be active in a way qualitatively similar to COP.

Animals↗

Protective effect of creatinol O-phosphate (COP) on some experimental arrhythmias in vitro and in vivo.

The activity of N-methyl-N-(beta-hydroxyethyl)guanidine O-phosphate (creatinol O-phosphate, COP) on two in vitro and in vivo experimental arrhythmias was investigated. The substance proved to be active in delaying the onset time of aconitine induced arrhythmias in guinea-pig atria. COP showed also a definite antagonizing activity against chloroform-induced ventricular fibrillation in mice.

Aconitine↗

The influence of calcium antagonists on endothelium.

Calcium antagonists possess, similarly to endothelotropic (vasotropic) drugs, a stabilizing effect on endothelium against the disrupting influence of citrate in rats. This was demonstrated with the new method for counting of circulating endothelial cells. The effect is dose related and the effective experimental dosages corresponded closely to the clinical dose range. The common link between both drug groups is probably the mediating effect of ionic calcium.

Animals↗