VIII. EFFECTS OF DEFICIENCY IN ANIMALS 293 



(4) lihriuogen, and (5) aiitithrombin. The following effects of scurvy with 

 respect to these primary factors have been observed : 



(1) Profhromhin. Sullivan el al}'^^ reported that total and partial deple- 

 tion of vitamin (' in the guinea pig resulted in no change in the prothrombin 

 level or acti\'ity of plasma diluted to one-eighth its original concentration. 

 Howe\'er, the clotting time of whole plasma was increased slightly. Marx 

 and Bayerle'^^ found, on the contrary, that in severe scurvy the prothrom- 

 bin time definitely is prolonged and that a sufficient supply of ascorbic 

 acid will l)ring it back to normal. 



(2) Tlirotnboplastin. The effect of scurvy on blood platelets has l)een re- 

 viewed in the section on blood. There are both qualitative and quantitative 

 problems with respect to blood platelets remaining to be solved. They are 

 of unquestionable importance in view of possible relations of thrombocyte 

 disturbances to vascular clotting. 



(3) Calcium. Hess and Killian'^^ obtained contradictory results in regard 

 to the calcium content of the blood in human scurvy. Their earlier studies 

 had shown a decrease in calcium but later they found normal val- 

 ues. Humphreys and Zilva'^" in studies with guinea pigs observed that the 

 blood calcium remains normal at least until the final stages of the disease. 

 Randoin and Michaux^^^ obtained similar results. This apparent constancy 

 of the blood calcium level during a period of profoundly disturbed metabo- 

 lism is doubtless in part possible because of withdrawals of calcium from the 

 bony trabeculae.^" 



(4) Fibrinogen. Randoin and Michaux^^^ and Marx and Bayerle^^^ found 

 an increased fibrinogen concentration in scurvy. Sullivan et al.^^^ also ob- 

 served that the fibrinogen content of guinea pig plasma increases markedly 

 with the onset of scurvy. Within two weeks after administration of vitamin 

 C the levels returned to normal. Salmon and May^*^ found that plasma 

 fibrinogen is considerably elevated in scurvy in the monkey. Other factors 

 such as hemorrhages and infection may contribute to the increase but do 

 not appear to account for it entirely. 



(5) Antithromhin. Quick'''^ holds that heparin does not by itself act as an 

 antithrombin but merely intensifies the action of normal antithromljin of 

 blood, i.e., serum albumin. If this is so, the diminution of plasma proteins'^^ 



"« W. R. Sullivan, E. O. Gangstad, and K. P. Link, /. Biol. Chem. 151, 477 (1943). 



1" A. F. Hess and J. A. Killian, Proc. Soc. Exptl. Biol. Med. 16, 4.3 (1918). 



ISO F. E. Humphreys and S. S. Zilva, Biochem. J. 25, 579 (1931). 



'*! L. Randoin and A. Michaux, Compt. rend. soc. biol. 194, 565 (1932). 



>62 J. D. Robertson, /. Roy. Soc. Arts 91, 358 (1943). 



•" W. R. Sullivan, E. O. Gangstad, and K. P. Link, J. Biol. Chem. 152, 307 (1944). 



1" R. J. Salmon and C. D. May, J. Nutrition 46, 515 (1952). 



1" A. J. Quick, Am. J. Clin. Pathol. 19, 1016 (1949). 



'56 J. Doi, ./. Oriental Med. 28, 209 (1938). 



