Journal of Okayama Medical Association
Published by Okayama Medical Association

Full-text articles are available 3 years after publication.


Harada, Hichiro
Thumnail 078_963.pdf 255 KB
While there are many basic and clinical studies on strychnine, reports on its derivatives are rare, except for a few reports by Koizumi and Chiyoda of our laboratory. They conducted general pharmacological studies on ethylstrychnine I, II, iodoethylstrychnine and strychnic acid ethylbetaine, new derivatives of strychnine. As a link in the series of such studies the author carried out some inverstigations on the effects of these three derivatives on blood clotting. and briefly presents the main results of the inverstigation. 1. Both ethylstrychnine I and II as well as iodoethylstrychnine, like their mother substance, strychnine, were found to shorten the blood clotting time of rabbits, and to enhance the blood coagulating elements. This effect was predominant in ethylstrychnine II followed by iodoethylstrychnine. The order of this potency coincides with that of the minimal lethal dose as found by Koizumi. 2. It was difficult to demonstrate this effect in vitro. Consequently, it is reasonable to assume that this effect to accelerate the blood clotting time is not due to a direct action of the drug on blood itself but is due to the bioreaction. 3. This accelerating effect on the blood clotting is almost completely inhibited by luminal, a brain-stem narcotics, but it is not affected by the premedication with yohimbine nor by the resection of bilateral, subdiaphragmatic splanchnic nerves. 4. It seems that this accelerating action is of a central nature and probably it is induced by an increase of coagulating elements such as fibrinogen and thrombin, resulting from the stimulating effect of the drug on the so-called blood coagulation-accelerative center in the diencephalon. In this instance, it appears that the splanchnic nerves are not involved in the transmission of excitation from the above metioned center to the peripheral region, but in this experiment it was impossible to demonstrate any evidence proving that the transmission of such stimuli is conducted via sympathetic accelerative fibers