328 RETROGRESSIVE CHANGES 



passes readily into the insoluble clot, myosin ; the other, which 

 coagulates at 56, constitutes the remaining four-fifths, is called 

 myosinogen (Halliburton), or myogen (v. Furth), and before be- 

 coming changed into myosin it passes through a soluble stage 

 called soluble myogen-fibrin, which is coagulated at the remark- 

 ably low temperature of 40. 



By analogy with fibrin- formation we should expect this 

 clotting also to be brought about by an enzyme, but this has 

 not been proved. Calcium is of influence, favoring coagulation 

 greatly, but its presence is not absolutely essential (v. Furth). 

 Of particular importance is the acid reaction of the dead 

 muscle. Normal muscle is amphoteric when at rest, but when 

 active the reaction becomes more and more acid, as it also does 

 when the circulation is shut off, and hence it increases greatly 

 after death. The acidity is due chiefly to lactic acid (although 

 the neutral phosphates may become converted into acid phos- 

 phates in the presence of the lactic acid, and thus seem to con- 

 tribute to the acidity), and may increase in twenty-four hours 

 after death by from 6.7 to 12.8 c.c. of ^ acid for each 100 

 grams of muscle (v. Furth l ). The same author found that 

 although the amount of acid might become in time sufficient to 

 cause coagulation of the muscle proteids by itself, yet actually 

 rigor mortis appears before the acidity has reached any such 

 degree. We may conclude that the acidity of the muscle 

 hastens the clotting, possibly by favoring some undemonstrated 

 coagulating enzyme, and in late stages it may become so great 

 as to precipitate the proteids that are not involved in the clot- 

 ting. This readily explains why the time of appearance of 

 rigor is so modified by the amount of muscle metabolism before 

 death. It is, indeed, possible to produce rigor in living animals 

 by transfusing a limb with slightly acid salt solution, 2 and in 

 strychnine-poisoning the muscular spasm may pass impercep- 

 tibly into rigor mortis. 



In all probability the disappearance of rigor mortis depends 

 upon beginning autolysis of the clot by the intracellular pro- 

 teases of the muscle, which act best in an acid medium. It is 

 improbable that the degree of acidity ever becomes so high that 

 the myosin is redissolved through a conversion into acid albumin 

 (syntonin), as was formerly supposed. 



1 Hofmeister's Beitr., 1903 (3), 543. 



2 The hardness of a limb from which the blood-supply has been shut off by 

 thrombosis or embolism, and also much of the cramp-like pain, is probably due 

 to rigor mortis in the muscles caused by acid formation under conditions of 

 sub-oxidation. 



