Prasad C M, Nair K G, Sheth U K
Res Commun Chem Pathol Pharmacol. 1980 Feb;27(2):405-8.
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.
在麻醉犬以及兔、豚鼠和大鼠的离体灌注心脏中研究了氯化镍对洋地黄诱导的心律失常的影响。结果表明,氯化镍在完整心脏和离体心脏中均能有效对抗洋地黄诱导的心律失常。窦性心律得以恢复,动物(已洋地黄中毒)的心血管状态最终恢复正常。若不使用氯化镍治疗,犬的心血管状态会逐渐恶化直至死亡。氯化镍单独对正常心脏没有任何显著影响。很可能镍离子在细胞膜位点与钙离子竞争,从而对抗洋地黄的毒性作用。氯化镍诱导的苹果酸和草酰乙酸活性增加也可能在逆转洋地黄毒性方面发挥作用。