124 Shiro Tashiro 



protoplasm is smashed, there occurs vigorous chemical changes, is 

 shown by several investigators. Fletcher 28 reports that injured 

 muscle gives off more C0 2 than the normal. 



Later he and Hopkins 29 discovered that muscle, under a similar 

 condition, is richer in lactic acid. 



Dr. Mathews has observed a similar activity in crushed eggs of 

 Arbacia. Quite accidently, I have discovered that a fresh nerve, too, 

 when crushed with the rough edge of a glass rod gives off more C0 2 . 

 This increase of gas production from the injured nerve, I take to be 

 due to mechanical stimulation. To test this hypothesis, I rendered 

 the nerve unexcitable by means of ether and 0.2 m. solution of KC1, 

 which is known to abolish excitability of a nerve. 30 



Under these conditions, I observed no increase of gas production 

 when the nerve is crushed. Therefore, the metabolism existing in 

 the living nerve must be accelerated by this stimulation when it is 

 injured. 



This interpretation, however, is not accordant with that of Fletcher 

 and Hopkins, on muscle. In studies of lactic acid formation in muscle, 

 they found that lactic acid is spontaneously developed, under anae- 

 robic condition, in excised muscle, and that fatigue due to contractions 

 of excised muscle is accompanied by an increase of lactic acid. In 

 an atmosphere of 2 , there is no survival development of lactic acid 

 for long periods after excision. From a fatigued muscle, placed in 

 62, there is a disappearance of lactic acid already formed. But this 

 disappearance of lactic acid, due to oxygen, does not occur, or is 

 masked, at supraphysiological temperature (e. g., at 30 ). Now 

 traumatic injury to an irritable muscle too produces a rapid develop- 

 ment of acid. Since, however, in this case the disappearance of lactic 

 acid due to O 2 does not occur, they conclude that one essential condi- 

 tion for this effect of oxygen appears to be the maintenance of the 

 normal architecture of the muscle. Thus they contend that the 

 increase of the lactic acid by mechanical injury is not due to stimula- 

 tion, but must be due to tissue destruction. 



They, however, did not determine, as 'far as I know, how much 

 the output of CO 2 is affected by treating the injured tissue with O 2 . 



28 FLETCHER: Journal of physiology, 1898-9, xxiii, p. 37. 



29 FLETCHER and HOPKINS: ibid., 1906-7, xxxv, pp. 261, 288. 



30 MATHEWS: This Journal, 1904, xi, p. 463. 



