394 RETROGRESSIVE CHANGES 



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 coagulated 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 "/lo acid for each 100 grams 

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

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

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

 before the acidity has reached any such degree. Verzar^^ saj^s that by 

 vital stains it can be shown that in vital contraction no precipitation 

 occurs, but it does take place in rigor mortis. Mcigs^^ 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 

 Fiirth and Lenk."^" When sufficient acid is formed in the muscle 

 the swelling may be so great that the structure of the muscle cell is 

 destroyed entirely, and it goes into the condition of ''waxy degenera- 

 tion."" 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,'^- and in strychnine-poisoning 

 the nauscular spasm may pass imperceptibly into rigor mortis. 



" Hofmeister's Beitr., 1903 (3), 543; see also Fletcher and Hopkins, Jour, of 

 Physiol., 1907 (35), 247; Wacker, Biochcm. Zeit., 1916 (75), 101. 



" ]5ioohom. Zeit., 1918 (90), (53. 



" Amor. Jour. Physiol., 1910 (26), 191. 



"OBiochem. Zeit., 1911 (33), 341; Wien. klin. Woch., 1911 (24), 1079. 



" Wells, Jour. Exper. Med., 1909 (11), 1. Corroborated ^hv Stcniinler, 

 Virchow's Arch., 1914 (216), 57. 



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

 throml)(jsi.s or embolism, and also much of the crami)-like pain, is probably due 

 to riffor mortis in the muscles caused by acid formation under conditions of sub- 

 oxidation. 



