292 ASCORBIC ACID 



depleted rather quickly, but a considerable amount remains in the white 

 cells until the signs of scurvy appear. ^"-^^^ In advanced scurvy this reten- 

 tion by the white cells is presumably, in part, a consequence of their origi- 

 nal high content as shown by Stephens and Hawley^^ and later confirmed 

 by Butler and Cushman.^^^- ^^^ It also appears that the leucocytes must have 

 a special capacity to absorb and retain the vitamin. 



(4) Platelets. Hess and Fish^^" reported that the number of blood platelets 

 was normal in infantile scurvy. Tobler^^i and Brandt^^^ observed an increase 

 in the platelets in human scurvy. Hess®* confirmed this observation and 

 stated that it was one which had not been anticipated in connection with 

 a disorder characterized by hemorrhage. However, several investiga- 

 ^Qj.gi29 , 143 . 144 found a thrombocytopenia associated with scurvy. Little is 

 known of the factors affecting blood platelets in the guinea pig. The need 

 of further study in this field is obvious. 



c. Coagulation Mechanism 



Hess and Fish^^" observed a slight diminution of the clotting power of 

 the blood in human scurvy which was not a result of insufficient calcium 

 in the diet. PresnalP^^ found that a 54 % delay in clotting time accompanied 

 the onset of scurvy in guinea pigs. Kuhnau and Morgenstern^*^ noted that 

 ascorbic acid had a marked accelerating effect on the m vitro coagulation 

 of the blood in the presence of minimal quantities of heavy metals. Hanut^^® 

 found that the intravenous injection of ascorbic acid (10 to 38 mg. per 

 kilogram) decreased the coagulation time of recalcified oxalated plasma 

 from 9 to 25 % but similar injections into guinea pigs beginning to show 

 signs of scurvy had little or no effect. Marx and Bayerle^^^ stated that the 

 coagulation time, determined on oxalated plasma, is normal in scurvy. The 

 general trend of evidence thus indicates that there is either no change or a 

 slight delay in clotting during the onset of scurvy. 



Since scurvy is a hemorrhagic disease, consideration should be given to 

 the factors concerned in the coagulation mechanism. The primary factors 

 involved are (1) prothrombin, (2) thromboplastin, (3) ionized calcium, 



1" M. Heinemann and P. M. Hald, /. Clin. Invest. 19, 469 (1940). 



138 A. M. Butler and M. Cushman, J. Biol. Chem. 139, 219 (1941). 



139 A. M. Butler and M. Cushman, J. Clin. Invest. 19, 459 (1940). 

 "» A. F. Hess and M. Fish, Am. J. Diseases Children 8, 385 (1914). 

 "1 W. Tobler, Z. Kinderheilk. 18, G3 (1918). 



"2 H. Brandt, Arch. Kinderheilk. 17, 395 (1919). 



1" S. Wasserman, Folia Haematol. 23, Part 1, 1 (1918). 



1" A. K. Presnall, /. Nutrition 8, 69 (1934). 



"^ J. Kuhnau and V. Morgenstern, Hoppe-Scyler's Z. physiol. Chem. 227, 145 (1934). 



"6 C. J. Hanut, Compt. rend. soc. biol. 121, 1338, 1341 (1936). 



1" R. Marx and H. Bayerle, Biochem. Z. 315, 366 (1943). 



