126 Shiro Tashiro 



It is known that normal saline stimulates frog's sciatic nerves. The 

 different rates at which CO 2 is produced from the different nerves 

 treated by various concentrations of KC1 is equally instructive. It 

 is known that when a nerve is placed in a molecular solution of KC1, 

 a stimulation takes place for a considerable time. Then it finally 

 becomes unexci table, 34 whereas, .2 m. KC1 solution abolishes nervous 

 excitability in a short time without primary stimulation. The CO 2 

 production follows exactly analogous to this. The nerve treated with 

 the stronger solution gives more CO 2 than that of a weaker solution. 

 This was true even after both nerves became unexcitable, showing 

 that the nerve must be giving off more CO 2 while being stimulated 

 by the stronger solution. Although my quantitative data are not 

 complete at this stage, this preliminary statement is sufficient to show 

 that the nerve chemically stimulated gives off more C0 2 . It may 

 be added in passing that the different solubility of CO 2 in the different 

 concentrations of these salts solutions cannot explain these results 

 solely by a physical interpretation, for there is not enough difference 

 in the solubility of C0 2 in dilute equimolecular solutions of KC1, 

 and NaCl, whose effect on C0 2 production is so divergent, the former 

 salt diminishing, the latter increasing it. 



Heat Stimulation. It may be recalled in Table I that high tem- 

 perature increases the output of CO 2 from the resting nerve. A 

 respiratory process should increase proportionally to the temperature. 

 Raising of temperature, however, not only increases the rate of res- 

 piration, but also (particularly by sudden changes of it) stimulates 

 the nerve. A very interesting fact is observed in connection with 

 the killing of the nerve. When the nerve is killed gradually by a 

 slow increase of temperature, it gives off more CO 2 than when killed 

 suddenly, the determination being made after both are killed. CO 2 

 production from the dead nerve under this condition must be due to 

 the diffusion of the gas which was formed previously, just as Fletcher's 

 dead muscle is charged with C0 2 gas. The different outputs of CO 2 

 between slowly killed and suddenly killed nerves cannot be accounted 

 for unless we assume that in one case, C0 2 is produced more while 

 being killed than in the other. Whether such increase of CO 2 produc- 

 tion, however, was due to the acceleration of normal respiration by 

 the slowly increasing temperature, or due to direct stimulation caused 



34 MATHEWS: loc. cit. 



