Dietmann K, Bartsch W, Gutekunst M
Arzneimittelforschung. 1977;27(3):589-93.
The antiarrhythmic and acute toxic actions of quinidine (Q) and dihydroquinidine (DHQ) were investigated in experiments in rats. 1. No significant difference was found between Q and DHQ with regard to the doses necessary to suppress electrically induced ventricular fibrillation in the heart (p greater than 0.05). 2. On oral administration, pure DHQ was slightly less toxic than pure Q. This difference is significant (p less than 0.05). It may be explained by a lower absorption rate of DHQ in the rat. Addition of 15 or 30% DHQ to Q did not produce any significant difference in the acute toxic doses (LD50) in comparison with pure Q (p greater than 0.05). 4. The results of a published clinical study showed that the antiarrhythmic actions of pure Q and "commercial" Q are the same with regard to quality, potency and duration. The frequency of side-effects after adminstration of the two alkaloids also did not differ. 5. Limitation or reduction of the DHQ content of pharmaceutical quality quinidine below a technically practicable level does not seem to be justified from a medical point of view from the results of the animal experiments presented and from the clinical study mentioned.
在大鼠实验中研究了奎尼丁(Q)和二氢奎尼丁(DHQ)的抗心律失常作用及急性毒性作用。1. 在抑制心脏电诱导室颤所需剂量方面,Q和DHQ之间未发现显著差异(p>0.05)。2. 口服时,纯DHQ的毒性略低于纯Q。这种差异具有显著性(p<0.05)。这可能是由于DHQ在大鼠体内的吸收率较低。与纯Q相比,在Q中添加15%或30%的DHQ在急性毒性剂量(LD50)方面未产生任何显著差异(p>0.05)。4. 一项已发表的临床研究结果表明,纯Q和“市售”Q在抗心律失常作用的质量、效力和持续时间方面相同。给予这两种生物碱后副作用的频率也没有差异。5. 从所呈现的动物实验结果和上述临床研究来看,从医学角度而言,将药用级奎尼丁中的DHQ含量限制或降低到技术上可行的水平以下似乎没有道理。