468 V. BLOOD LIPIDS 



in arterial walls was likewise demonstrated in in vitro tests of Wilens/ 29 

 who reported that a visible lipid retention occurred if normal human blood 

 serum was filtered through the walls at normal arterial pressures for twenty- 

 four hours or longer. It was estimated that 2 to 38% of the cholesterol 

 was retained intramurally. It was suggested that atherosclerosis results 

 from filtration of serum through the walls of the artery; the major portion 

 of the cholesterol fails to enter the arterial intima, due to its linkage with 

 large protein molecules. It is postulated that only free cholesterol can 

 pass into the arterial walls. 



Although there is considerable indication that cholesterol deposition is 

 the primary cause for the development of atheromas, Peters and Van 

 Slyke 202 do not subscribe to this hypothesis. The latter investigators 

 state that the presence of cholesterol in the atheromatous patches does not 

 prove that a hypercholesterolemia or any disturbance in cholesterol me- 

 tabolism has been the cause of the deposition. In fact, Chernick, Srere, 

 and Chaikoff, 730 as well as Werthessen et aU n have shown that cholesterol 

 can be synthesized in the arterial wall. 



b'. Dietary and Other Factors Related to the Formation of Atheromas: 

 A large number of workers have shown that a diet high in cholesterol causes 

 the development of atherosclerosis in rabbits, 732 " 734 in chickens, 735,736 and 

 in geese. 737 Wissler and co-workers 738 reported that it was possible to 

 produce lipomatous lesions in the coronary arteries of rats fed for a year on 

 a diet containing a high proportion of lard and a high level of choline, with 

 or without added cholesterol. On the other hand, no significant lesions 

 were noted in rats receiving similar diets, for the same period, when corn 

 oil was substituted for the lard, or in rats on a commercial stock diet. 

 The incidence of the lesions was correlated with the progressive changes in 

 the lipid components of the blood. Although Anitschkow 739 was unable 



729 S. L. Wilens, Science, 114, 389-393 (1951). 



730 S. Chernick, P. A. Srere, and I. L. Chaikoff, J. Biol. Chem., 179, 113-118 (1949). 



731 N. T. Werthessen, L. J. Milch, R. F. Redmond, L. L. Smith, and E. C. Smith, Am. J. 

 Physiol, 178, 23-29 (1954). 



732 N. Anitschkow and S. S. Chalatow, Zentr. allgem. Pathol, u. path. Anat., 24, 1-9 

 (1913). 



733 O. J. Pollak, Am. Heart J., 38, 459-460 (1949). 



734 A. Kuntz and N. M. Sulkin, Arch. Pathol, 47, 248-260 (1949). 



735 L. Horlick, and L. N. Katz, Am. Heart J., 38, 336-349 (1949). 



736 J. E. Peterson and A. E. Hirst, Circulation, 3, 116-119 (1951). 



737 J. B. Wolffe, A. S. Hyman, M. B. Plungian, A. D. Dale, G. E. McGinnis, and M. B. 

 Walkow, /. Gerontol, 7, 13-23 (1952). 



738 R. W. Wissler, J. L. Collins, M. Schroeder, and K. Soules, Federation Proc, 12, 

 407 (1953). 



739 N. Anitschkow, Verhandl deut. pathol, Ges., 20, 149-154 (1925). 



