HEMORRHAGE 293 



times, Austrian) more viscous than water, chiefly because of the 

 corpuscles and the dissolved proteins. This viscosity does not vary 

 directly Avith the specific gravity or the hemoglobin, but is closely 

 related to the number of red corpuscles (Burton-Opitz) ; laking the 

 corpuscles increases the viscosity considerably. ^lost salts increase 

 the viseosit}', but some, especially iodides, are said to reduce it. Car- 

 bon dioxide increases viscosity greatly, even when in amounts possible 

 in the circulating blood. Anemia decreases the viscosity, approxi- 

 mateh' in proportion to the number of corpuscles ; polycythemia is ac- 

 companied by a corresponding increase ; leukemia, because of anemia, 

 shows a decrease ; in nephritis there may either be an increase or a de- 

 crease in the viscosity, not corresponding in any way to the blood pres- 

 sure. Cardiac disease with edema shows low viscosity" because of the 

 anemia and hydremia, but if there is polycythemia and no edema the 

 viscosity may be high. Jaundice, causes an increase, diabetes gives 

 variable results. Typhoid causes no characteristic change beyond that 

 resulting from anemia, and in pneumonia the cyanosis and salt reten- 

 tion usually cause an increase (Austrian). Gullbriug ^^'^ found the 

 viscosity to vary directl}' with the per cent, of neutrophiles. 



HEMORRHAGE 



Hemorrhages result from an altered condition in the vessel-walls, 

 which may be due either to trauma or to chemical injuries. Of 

 the chemical agencies causing hemorrhages, bacterial products are the 

 most important practically, but manj' poisons, such as phosphoinis, 

 formaldehyde, phytotoxins (ricin, abrin, and crotin), and zootoxins 

 (snake venoms) cause numerous and abundant hemorrhages. For- 

 merh', the tendency was to ascribe hemorrhages from the above causes 

 to mechanical injury of the vessels by thrombi, or by emboli of ag- 

 glutinated corpuscles, but the work of Flexner " has shown that 

 venoms cause hemorrhages by injuring the capillary walls, so that 

 actual rents are produced by the intravascular pressure, and it seems 

 highly probable that hemorrhages are produced by other chemical 

 substances in a similar way. We may, therefore, refer such hemor- 

 rhages to an endotheliotoxic action of the poison, or to a solvent effect 

 upon the intercellular cement substance. In the case of ordinary 

 chemical poisons the endotheliotoxic action is not specific, but with 

 some of the toxins it seems to be quite so; for example, rattlesnake 

 venom contains an endotheliotoxic substance (hemorrhagin) , which 

 seems to be a specific poison for endothelium, and which is the most 

 dangerous constituent of the venom. If we immunize animals against 

 tissues containing iiiucli endotlielium ( c. g., lymph-glands), their serum 



Austrian, Johns Hopkins Hosp. Bull., 1911 (22), 9. See also Traube, Internat 

 Zeit. phvsik.-chem. Biol., 1014 (1), 380. 



isaBeitr. klin. Tuberk., 1014 (30), 1. 



16 Univ. of Penn. Med. Bull., 1902 (15), 355. 



