VII. VITAMIX A DF-FiriEXCY IX AXIMALR 135 



iivicntly tliroinhi in the .sinuses of clumped red cell origin.' Lymph nodes 

 of all species, usually from stmie one or several locations, contained red 

 blood corpuscles in their siiuises, most markedly so in regions adjacent to 

 hemorrhages. 



The bone marrow in all species showed no constant change or evidence of 

 specific vitamin A influence, ^'ascular lesions in arteries and veins were 

 found in one of two dogs^ and in a few of many rats studied, but whether 

 or not these lesions are related to the hypoprothroml)inemia associated 

 with excess vitamin A remains hypothetical. 



D. PRENATAL CONSEQUENCES OF VITAMIN A DEFICIENCY 



Severe maternal vitamin A deficiency in pigs and rats results in death 

 and resorption of the fetus. Both maternal and placental epithelia degen- 

 erate.'*' If the deficiency is not complete, the fetus may go to term and 

 show abnormalities which can be related to arrestment of the skeleton and 

 various organs. The first studies in this field were by Hale upon pigs."*^ 

 Five-month-old gilts were kept on a vitamin A-deficient diet until signs of 

 the deficiency were apparent (IGO to 192 days). They were then bred to 

 normal sires and kept on the deficient diet for 30 days, after which cod 

 liver oil was given in order to permit completion of gestation. Otherwise, 

 death of the fetuses resulted. Fetuses carried to term showed a variety of 

 defects, including various stages of arrestment of formation of the eyes 

 to complete lack of eyeballs, harelip, cleft palate, misplaced kidneys, and 

 extra ear-like growths. Warkany*^' *"* in rats obtained arrestment of develop- 

 ment of ej^es, pleural cavities, lungs, heart, kidneys, testes, and diaphragm. 

 Anomalies of the heart and blood vessels, all correlatable to arrestment of 

 development at various embryological periods and similar to cardiovascular 

 abnormalities of humans, have been described in the young of vitamin A- 

 deficient rats.''^' "" 



An interesting result of maternal vitamin A deficiency in the rat is that 

 described by Andersen,'^ who discovered that the expression of a "genetic 

 trait" — congenital diaphragmatic hernia — in an inbred stock of albino rats 

 could be enhanced (incidence 18.9%) or depressed (incidence of 0.9%) by 



^5 K. E. Mason, Am. J. Anat. 57, 303 (1935). 



^« F. Hale, Am. J. Ophthalmol. 18, 1087 (1935). 



"J. Warkany, Vitamins and Hormones 3, 73 (1945). 



« J. Warkany and C. B. Roth, ./. Nutrition 35, 1 (1948). 



^9 J. G. Wilson and S. Barch, Proc. Soc. Exptl. Biol. Med. 72, 687 (1949). 



60 J. G. Wilson and J. Warkany, Pediatrics 5, 708 (1950). 



61 D. IL .\ndcrsen, Am. J. Pathol. 25, 163 (1949). 



