Abstract
Since Twitty and coworkers 1 demonstrated the existence of a powerful toxin in the eggs and embryos of the amphibian Triturus, investigations have been conducted to determine its physical and chemical characteristics and physiological effects.
Horsburgh, Tatum and Hall 2 showed that the toxin produces death in mammals, usually preceded by convulsions, by direct depression of the central nervous system. These workers demonstrated that while paralysis of the respiratory nerves and muscles occurs as a result of depression of the centers, the toxin paralyzes somatic motor nerves and skeletal muscle generally. Vagus and splanchnic nerve responses are abolished, but not, according to the evidence obtained, those of the cervical sympathetic trunk. The experiments gave no evidence of an effect on cardiac or smooth muscle since arterial pressure responses to adrenalin were not affected. The arterial fall in pressure was attributed to vasomotor paralysis.
Fuhrman and Field 3 demonstrated that the toxin has little effect on the oxidative metabolism of nervous tissue in experiments treating rat brain in vitro with the toxin.
Although Horsburgh, Tatum and Hall 2 were unable to observe any effects of the toxin in the concentrations used on cardiac tissue, it seemed of interest to determine whether at higher concentrations the toxin might not have some direct effect on the beating heart. It seemed possible that further light might be cast on the action of the toxin by testing its effects on rhythmically contracting mechanisms in which it might be possible to separate effects on the pacemaker, on conduction and on contractility. Accordingly both mechano- and electrocardiograms were made of the heart of Rana pipiens under treatment with toxin.
The toxin, kindly provided by Dr. Tatum, was dry and had been computed to be of a potency of approximately 3500 mouse units per g.
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