760 XII. VITAMINS K 



which may be defined as alimentary. A number of investigators reported 

 that the prothrombin level is low at birth, ^'^•^' or, if normal, ^^'^^ rapidly 

 drops during the early days of life,^* presumably because of the lack of 

 vitamin K in the diet, and of any alimentary source, since vitamin K 

 cannot be synthesized in the sterile meconium of the gastrointestinal tract. 

 When food is taken, recovery may occur spontaneously, presumably due to 

 the establishment of suitable intestinal flora.^^~^^ 



5. The Transport of Vitamin K from the Intestine to the Tissues 



There is little direct information as to the mechanism l)y which the 

 vitamins K are distributed to the various tissues of the animal. Since 

 increased amounts of the vitamin occur in the liver and other tissues after 

 their administration, this must mean that they are transported either by 

 the blood stream or by the lymphatics, or both. Since the natural forms 

 are insoluble in water, and are soluble only hi fat, it would seem probable 

 that the pathwaj^ of transport from the intestine would be the same as that 

 for other fat-soluble vitamins and for fat itself, namely the lacteals, the 

 intestinal lymphatics, and ultimately the thoracic duct, from which it is 

 emptied into the blood stream. 



Evidence for the lymphatic route has recently been adduced by the use 

 of a new operati\'e procedure de^'ised by Bollman, Cain, and Grindley**^ 

 for the collection of lymph from the liA'er. When the intestinal lymph was 

 drained, a vitamin K deficiencj^ could be produced within a short period.^" 

 One must interpret the.se data as evidence that the natural forms of vitamin 

 K are transported via the lymph, and that an insufficient quantit}^ is carried 

 via the portal system to counteract the hypoprothrombinemia. Millar 

 et al.,^^ who used radioactive vitamin Ki, reported the presence of the vitamin 

 in the intestinal lymph of rats and dogs. Radioactive products were also 



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 (1937). 



81 K. Kato and H. G. Poncher, /. Am. Med. Assoc, 114, 749-753 (1940). 



82 K. K. N3'gaard, Ada Ohslet. Gi/necol. Scand., 19, 361-370 (1939). 



83 C. A. Owen, G. R. Hoffman, S. E. Ziffren, and H. P. Smith, Proc. Soc. ExpLl. Biol. 

 il/ec?., .4;, 181-185 (1939). 



84 A. J. Quick, Wisconsin Med. J., 38, 746 (1939). 



85 A. J. Quick and A. M. Grossman, Am. J. Med. Sci., 199, 1-9 (1940). 



86 A. J. Quick and A. M. Grossman, Proc. Soc. Exptl Biol Med., 40, 647-648 (1939). 



87 A. J. Quick and A. M. Grossman, Proc. Soc. Exptl. Biol. Med., 4I, 227-228 (1939). 



88 J. L. BoUman, J. C. Gain, and J. H. Grindlev, ./. Lab. Clin. Med., 33, 1349-1352 

 (1948). 



88 J. D. Mann, F. 1). Mann, and J. L. BoUman, Am. ./. Phi/siol., 1.58, 31 1-314 (1949). 

 ^° G. J. Millar, J. A. Leddy, and L. Fisher, A7A' International Physioloyicnl Congress, 

 Montreal, 1953, Abstracts of Communications, pp. 618-619. 



