RIGOR MORTIS 391 



muscle will thou be found to react to stimuli. This indicates that the 

 chemical chano:es of rigor mortis are not very profound.^** 



The chemistry of the changes involved in rigor mortis has been 

 a much-contested problem. Two chief doctrines have been sup- 

 ported : one that rigor was not essentially different from ordinary 

 muscular contraction except in degree, and perhaps due to a loss 

 of inhibition to contraction. The other looks upon it as a coagula- 

 tion similar to the coagulation of the blood ; and this idea, it may be 

 said, has had the most general acceptance. Brlicke in 1842 supported 

 this view, and in 1859 Kiihne extracted from muscle a plasjua which 

 coagulated like ordinary blood plasma. The protein which formed 

 the clot is called myosin, and its coagulable antecedent, myosinogen. 



This experiment ha.s been since repeatedly verified and amplified, 

 especiall}' by v. Fiirth and by Halliburton," who have separated 

 more definitely the proteins concerned in coagulation, and found 

 them to be globulins. There seem to be two : one, coagulating at 47°, 

 called paramyosinogen (Halliburton), constitutes but about one-fifth 

 of the total clotting globulin, and passes readily into the insoluble 

 clot, myosin: the other, which coagulates at 56°, constitutes the re- 

 maining four-fifths, is called myosinogen (Halliburton), or myogen 

 (v. Fiirth), and before becoming changed into myosin it passes 

 through a soluble stage called soluble myogen-fibrin, which is coagu- 

 lated at the remarkably 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. Fiirth). 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 acidity 

 increases greatly after death. The acidity is due chiefly to lactic 

 acid (although the neutral phosphates may become converted into 

 acid phosphates in the presence of the lactic acid, and thus seem 

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

 after death by from 6.7 to 12.8 c.c. of "/^o acid for each 100 grams 

 of muscle (v. Fiirth -°). The same author found that although the 

 amount of acid might become in time sufScient to cause coagula- 

 tion of the muscle proteins by itself, yet actually rigor mortis appears 

 before the acidity has reached any such degree. Meigs -^ advanced 

 the hypothesis that the rigor is due to the swelling of the muscle col- 

 loids under the influence of acids, a view which is accepted by von 



isSoe Mangold. Pfliiper':, Arch., 1003 (Ofi), 4nS. 



19 "Chemistry of ^fuscle and Xerve." 1004. 



20 Hofnieister's Beitr., 1003 (3), r)43 : see also Fletcher and Hopkins, Jour, of 

 Phvsiol.. 1007 (3.5), 247; Wacker. Biochem. Zeit., 1016 (75), 101. 



2iAmer. Jour. Physiol., 1010 (26), 101. 



