Tetrodotoxin 중독가토(中毒家兎)의 심전도학적(心電圖學的) 연구(硏究)

An Electrocardiographic Study on Tetrodotoxin Intoxicated Rabbits

Tetrodotoxin (TTX) is the purified active principle responsible for tetrodon (Puffer-fish) poisoning which has long been known in the Orient. The pharmacological actions of TTX have been rather extensively investigated. Two of the most prominent effects of intravenousely administered TTX are severe hypotension and respiratory paralysis resulting from its depressant actions on tissues. This depressant actions of TTX in turn result from the selective inhibition of sodium-carrying mechanism which is essential to generation of the action potential. TTX differs from local anesthetics in that it does not affect potassium conductance. Although the mechanism of the hypotensive action of TTX remains a subject of controversy, most investigator agree that TTX-induced hypotension is caused by alteration in the blood vessels rather than the heart. Not only the study on the effects of TTX on cardiac function is meager but the results of reported works are often contradictory. The present study was undertaken to investigate the effect of TTX on the electrocardiogram of the rabbit and to compare them with well known electrocardiographical characteristics found in digitalis and quinidine intoxicated animals. The results obtained from the present study are summarized as follows. 1. No changes were found in P-R interval and QRS duration after i.v. administration of $1.0\;{\mu}g/kg\;to\;1.5\;{\mu}g/kg$ TTX to the animals. It is obvious that there were no conduction disturbance between atria and ventricles as well as in the ventricular tissue. 2. In $1.0\;{\mu}g/kg$ TTX group, S-T interval and T-P segment were not changed whereas marked changes were observed in $1.5\;{\mu}g/kg$ TTX group. 3. The first and second degree A-V blocks appeared in the $2.0\;{\mu}g/kg$ TTX group. 4. TTX differs from digitalis and quinidine in that it does not cause S-T interval depression and T-wave inversion. In contrast with digitalis, TTX caused Q-T interval prolongation.