164 AN AMERICAN TEXT-BOOK OF PHYSIOLOGY. 



as Fiirth says, to myogen-fibrin and niyosin-fibrin ' by the action of myosin 

 ferment. The change can go on in the absence of calcium, but whether this 

 is essential to the formation of the ferment is not yet known. The myosin 

 ferment is not the same as fibrin ferment, since neither can do the work of 

 the other. Moreover, fibrin ferment is destroyed at 75°-80° C. and myosin 

 ferment is not destroyed till 100° C. 



The chemical change which results in the formation of myosin is different 

 from that which produces fibrin. The clotting of muscle-plasma and the 

 formation of myosins are accompanied or closely followed by the production 

 of an aeid, while no such change occurs during the coagulation of blood-plasma. 

 In the earlier stages of clotting the acidity may be due in part to acid potas- 

 sium phosphate, but the final acidity is chiefly due to lactic acid. The source 

 of the lactic acid has not been definitely made out. The view that it comes 

 from glycogen is made questionable by Bohm's 2 observation that the amount 

 of glycogen is not lessened in rigor ; besides, the muscles of starving animals 

 become aeid when entering into l'igor, although, as Bernard found, they con- 

 tain no glycogen. Bohni concluded that the sarcolactic acid may be formed 

 from the proteids. Probably both glycogen and proteids can yield lactic 

 acid. 



Some writers have thought that the coagulation of the muscle was due to 

 the formation of an acid by the dying muscle. This is unlikely, although the 

 presence of acid, like that of many other substances, quinine, eaffein, digitalin, 

 veratrin, hydrocyanic acid, ether, chloroform, etc., which lead to altera- 

 tions in the conditions of the normal muscle-substance, may hasten the proc- 

 ess. Apparently, anything which causes a deterioration of the muscle-sub- 

 stance, chemical reagents, drugs, or the products of fatiguing work, hastens 

 the coming on of rigor. On the other hand, anything which helps maintain 

 the normal constitution of the muscle appears to postpone the change. Thus 

 Latimer 3 reports that the circulation of dextrose through fatigued muscle 

 largely does away with the effect of fatigue to hasten rigor mortis. Nor is 

 this because fatigue products are washed out of the muscle, for the circula- 

 tion of other fluids through the muscle, whether neutral, acid, or alkaline, 

 fails to have the effect. 



Rigor Caloris. — If a muscle be heated beyond its normal temperature, its 

 irritability is increased, and it undergoes rapid katabolic changes which lead 

 to its death. These changes, if sufficiently rapid, may bring about a con- 

 traction of the muscle, and this contraction, involving the different fibres of 

 the muscle to different degrees, may be continued without break by the con- 

 traction that is peculiar to rigor mortis; in addition to this, if the temperature 

 is raised sufficiently, then' will be a heat precipitation of the various proteids 

 of the muscle, which will lead to a still further shortening, the contraction 



1 Faith: Archiv fur experimenteUe Paihologie umd Pharmakologie, 1895, xxvi. 231; and 1896, 

 .xxxvii. 389. 



Pfluger*8 Archiv, 1880, Bd. xxiii. 8. 44. 

 8 Latimer: American Journal of Physiology, 1899, ii. p. 29. 



