380 RETROGRESSIVE CHANGES 



dasch^^ find changes in the brains of electrocuted criminals, which 

 indicate a sudden liberation of gas about the blood vessels, along which 

 the current passes. The amperage seems to be far more important in 

 determining the effect of a current than the voltage or wattage.^® 



Chemicals cause cell death whenever they are of such a nature as 

 either to coagulate the cell proteins or to destroy its enzymes. The 

 action of such substances as sulphuric acid, strong caustics, etc., 

 hardly calls for explanation. Phenol (carbolic acid) may cause ne- 

 crosis and gangrene even when in very dilute solution; this appears 

 to be due more to the production of hyaline thrombi of agglutinated 

 red corpuscles in the capillaries than to direct action upon the cells. 

 In some unpublished experiments on the subject of "carbolic acid 

 gangrene," I found this action of phenol very striking when dilute 

 solutions were placed on the web of a frog's foot, under the micro- 

 scope; as soon as the solution penetrated to a capillary, stasis with 

 fusion of the corpuscles occurred in a very few seconds. Similar 

 results have been obtained by Rosenberger.^^ Some poisons seem to 

 cause necrosis without destroying the autolytic enzymes, in which 

 case the cells are rapidly digested; at least, such an hypothesis seems 

 -to explain best the changes seen in the liver in chloroform poisoning, 

 acute yellow atrophy, eclampsia, etc.^* Not all poisons, b}^ any 

 means, cause cell death — tetanus toxin, morphine, and other alkaloids 

 cause death of the individual as a whole without usually causing pri- 

 mary necrosis of any of the cells. Cell death does not necessarily de- 

 pend upon destruction of all the cellular enzymes, as has been pointed 

 out previously. Thus, bacteria may be killed by many chemicals 

 which seem not to affect their autolytic enzymes seriously. Any con- 

 siderable excess of either H or OH ions is incompatible with cell life, 

 and it is possible that at times the production of acids within a cell 

 may be sufficient to cause death;^^ e. g., in the kidney in acute nephritis 

 (M. H. Fischer), or in the muscle in waxy degeneration ( Wells). ^° 

 It is quite probable that many of the poisons act by interfering with 

 the oxidative capacity of the cells; this seems almost certain in the 

 case of chloroform necrosis, and even bacterial poisons (diphtheria 

 and typhoid) were found by Pitini^^ to decrease the oxidizing power 

 of the cells. 



The term, "protoplasmic poison," has been variously used and de- 

 fined. Kunkel says that a protoplasmic poison "is a poison which, 



86 Amer. Jour. Med. Sci., 1912 (144), 341. 



89 Jellinek, Wien. klin. Woch., 1913 (26), 1793. 



8' Verb. Phys. Med. Gesellsch. z. Wurzburg, 1900, vol. 34. 



88 Wells, Jour. Amer. Med. Assoc, 1906 (46), 341. 



8" The partial protection afforded by a rich carbohydrate diet against the 

 necrogenic action of chloroform, phosphorus and renal poisons, as observed by 

 Opie and Alford (Jour. Exp. Med., 1915 (21), 1), may depend on the antiketogenic 

 effect of carbohydrates. 



»" Jour. Kxp. Med., 1909 (11), 1. 



»' Biochem. Zeit. 1910(253.257. 



