Reversal of digoxin induced cardiac arrhythmias by nickel chloride.
The effect of NiCl2 on digoxin induced cardiac arrhythmias were studied in anesthetized dogs and in isolated perfused hearts of rabbits, guinea pigs and rats. The results indicate that NiCl2 can effectively antagonize the digoxin induced cardiac arrhythmias in both intact as well as in isolated hearts. Sinus rhythm was restored and the cardiovascular status of the animal (which was digitoxic) eventually restored to normal. When not treated with NiCl2 the cardiovascular status of the dogs was progressively worsened leading to death. NiCl2 alone did not have any marked effect in normal hearts. It is likely that Ni2+ might be competing with Ca2+ at the cell membrane sites thereby antagonizing the toxic effects of digoxin. It is also possible that an increase in malic acid and oxaloacetic acid activity induced by NiCl2 may play a role in reversing the toxicity of digoxin.
D000818:Animals; D001145:Arrhythmias, Cardiac / Q000139:chemically induced / Q000503:physiopathology*; D004077:Digoxin / Q000037:antagonists & inhibitors* / Q000494:pharmacology; D004285:Dogs; D005260:Female; D006321:Heart / Q000187:drug effects; D066298:In Vitro Techniques; D008297:Male; D009532:Nickel / Q000494:pharmacology*; D013045:Species Specificity; D013997:Time Factors
D004077:Digoxin; D009532:Nickel