Williams J F, Potter R D, Mathew B
Am Heart J. 1983 Jan;105(1):21-5. doi: 10.1016/0002-8703(83)90273-9.
Digitalis toxicity in vivo generally is recognized by the appearance of cardiac arrhythmias but in vitro by a decline in myocardial performance. To determine whether concentrations of digitoxin producing cardiac arrhythmias in intact animals also produce a decline in myocardial performance directly, three groups of adult cats were studied. One received digitoxin daily until arrhythmias developed (toxic group), the second sufficient digitoxin to produce an inotropic effect without arrhythmias (nontoxic group), and the third was untreated. Peak isometric force and maximal dF/dt of isolated right ventricular papillary muscles were significantly greater in nontoxic muscles (3.9 +/- 0.4 gm/mm2 and 21.3 +/- 1.7 gm/mm2 . sec-1). Values in toxic muscles were similar to untreated ones (2.8 +/- -.6 gm/mm2 and 19.0 +/- 3.2 gm/mm2 . sec-1). Acetylstrophanthidin (2 X 10(-8) M) resulted in an increase in peak force and max dF/dt in nontoxic muscles, whereas myocardial performance changed minimally in untreated muscles and declined in 8 of 10 toxic muscles. We conclude that electrical and mechanical toxicity induced by digitoxin frequently coexist.
洋地黄体内毒性通常通过心律失常的出现来识别，而体外毒性则通过心肌性能下降来识别。为了确定在完整动物中产生心律失常的洋地黄毒苷浓度是否也会直接导致心肌性能下降，对三组成年猫进行了研究。一组每天接受洋地黄毒苷直至出现心律失常（中毒组），第二组接受足以产生正性肌力作用但无心律失常的洋地黄毒苷（无毒组），第三组未接受治疗。无毒肌肉中分离的右心室乳头肌的峰值等长力和最大dF/dt显著更高（分别为3.9±0.4 g/mm²和21.3±1.7 g/mm²·秒⁻¹）。中毒肌肉中的值与未治疗肌肉相似（分别为2.8±0.6 g/mm²和19.0±3.2 g/mm²·秒⁻¹）。乙酰毒毛花苷（2×10⁻⁸ M）导致无毒肌肉的峰值力和最大dF/dt增加，而未治疗肌肉的心肌性能变化最小，10只中毒肌肉中有8只下降。我们得出结论，洋地黄毒苷引起的电毒性和机械毒性经常共存。
