IlKMOh-h'/fACK 29;i 



from the inability of the blood to carry CO2. The blood and tissue jjrotcinf 

 also can bind much of either H or OH ions," so that the preservation of neutrality 

 is elaborately guarded. In the tissues, because of the profluc.tion of acids during 

 metabolism, the Il-ion concentration is slightly higher than that i)f the blood, being 

 estimated by Michaelis at exact neutrality, 1.5 X 10"'. Presumably one impor- 

 tant purpose of the e.xact regulation of reaction is to provide proper conditions for 

 enzyme action. 



The alkali of the blood exists in part as alkaline salts, carbonate and phosphate 

 (the diffusible alkali), and partly combined with protein {non-diffusible alkali). 

 As the corpuscles are richer in diffusible alkali than the plasma or serum, the num- 

 ber of corpuscles modifies the alkalinity of the blood decidedly. Much importance 

 is attached to the question of the alkalinity of the blood for two reasons: first, in 

 certain conditions of disease the blood contains so much of organic acids that the 

 alkali is partly saturated and the power of the blood to carry CO., is lessened, 

 with serious results (see "Acid Intoxication," Chap, xx); and, second, the bacteri- 

 cidal power of the blood is found to vary according to its alkalinity. In fact, 

 metabolic activity seems generally to be favored V\v certain degrees of alkalinity; 

 for example, J. Loeb^- found that sea-urchin eggs develop with much greater 

 rapidity if a small amount of OH ions is free in the .-:ea-water. Brandenburg'^ 

 states that the non-diffusible alkali varies according to the amount of protein in 

 the blood; in pneumonia and acute nephritis he found it low. In cancer the 

 titrable alkalinitj' is distinctly increased, and Moore and Walker'* hold that this is 

 due to an increased alkalinity of the proteins of the blood. Awerbach'* claims that 

 in severe high fevers the bactericidal effect of the blood alkalinity is increased 

 (see also "Passive Congestion" for further discussion concerning the relation of 

 alkalinity to bactericidal power). 



Viscosity of the Blood." — Normal blood is about five times (4.5 times, Austrian) 

 more viscous than water, chiefly because of the corpuscles and the dissolved pro- 

 teins. This viscosity does not vary directly with the specific gravity or the hemo- 

 globin, but is closely related to the number of red corpuscles (Burton-Opitz) ; 

 laking the corpuscles increases the viscosity considerably. Most salts increase 

 the viscositj', but some, especially iodides, are said to reduce it. Carbon dioxide 

 increases viscosity greatly, even when in amounts possible in the circulating blood. 

 Anemia decreases the viscosity, approximately in proportion to the number of 

 corpuscles; polj'cythemia is accompanied by a corresponding increase; leukemia, 

 because of anemia, shows a decrease; in nephritis there maj' either be an increase 

 or a decrease in the viscosity, not corresponding in any way to the blood pressure. 

 Cardiac disease with edema shows low viscosity because of the anemia and hydre- 

 mia, but if there is polycj'themia and no edema the viscosity may be high. .Jaun- 

 dice causes an increase, diabetes gives variable results. Typhoid causes no charac- 

 teristic change beyond that resulting from anemia, and in pneumonia the cyanosis 

 and salt retention usually cause an increase (Austrian). Gullbring'" found the 

 viscosity to vary directly with the per cent, of neutrophiles. As blood viscosity 

 depends largely upon the corpuscles, it increases with reduction in the size of the 

 lumen of the tube through which it passes, unlike a true solution; hence with narrow 

 capillaries the viscosity is abnormally high until we reach the point where the 

 corpuscles plug the capillary. 



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 arc the 



11 See Robertson, Jour. Biol. Chem., 1909 (6;, 313; 1910 (7), 351. 



1= Arch. f. Entwicklungsmechanik, 1898 (7), 631. 



13 Deut. med. Woch., 1902 (28), 78; Zeit. f. klin. Med., 1902 (-45), 157. 



1^ Biochem. Jour., 1906 (1), 297; good discus.sion of blood reaction. 



15 Med. Obosrenije, 1903, p. 596. 



1^ Review of literature by Determann, Zeit. klin. Med., 1910 (70), 185; also 

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

 Zeit. physik-chem. Biol., 1914 (1), 389. 



'" Beitr. klin. Tuberk., 1914 (30), 1. 



