HANDBOOK OF PHYSIOLOGY 



CIRCULATION II 



cated that if any atheroma lipid comes from local 

 synthesis, it is probably only the phospholipid com- 

 ponent. 



One other major question relating to the intimate 

 pathogenesis of the atherosclerotic lesion remains 

 unanswered: What are the mechanisms for incorpora- 

 tion of lipid into cells to form lipophages? In each of 

 the hypotheses mentioned above for the pathologic 

 background of the early lesion, the common hall- 

 mark, whether primary or secondary in time and in 

 importance, is the lipophage or foam cell (156), the 

 very name of which suggests incorporation of lipid 

 (fig. 1). The knowledge of the exact derivation of the 

 foam cell is fundamental to a better understanding 

 of atherogenesis. 



Is anabolic activity neccsary for the accumulation 

 of lipid in the cellular cytoplasm (as opposed to an 

 engulfing mechanism)? One clue may be that the 

 lipophage differs from the lipocyte, or adipose-tissue 

 cell, by the former's higher content of protein and 

 lipids other than neutral fat. Current attempts to 

 studv this problem bv in vitro tissue culture tech- 

 niques (180) may help to answer this and other 



important questions about the role of the lipophage 

 in atherogenesis. 



Do lipophages form simply because there is lipid 

 material available to be engulfed or phagocytized? 

 In favor of this concept is the observation that lipo- 

 phages are not peculiar to the atherosclerotic lesion; 

 they are found as part of the detritus in hemorrhage 

 into the various tissues; they are found as apparent 

 scavengers in lipoid pneumonia; they occur in 

 degenerating tumors; they are found experimentally 

 after the subcutaneous injection of cholesterol sus- 

 pensions; and they are found in the lipoidoses 

 (Niemann-Pick, etc.) in massive accumulations in- 

 volving the reticuloendothelial system. In most, if 

 not all, of these situations, it is reasonable to assume 

 that a scavenging attempt to rid the tissue of a local 

 excess of lipid is involved. 



Yet, in the atheromatous lesion, there appears to 

 be an additional element — one of accumulation. A 

 single minute atheroma, invisible to the naked eye, 

 is made up of a tremendous number of lipophages, 

 packed together in the subintima in such volume as to 

 displace adjacent normal tissue and to project into 



>* 



fig. I. Photomicrograph of a 

 foam cell protruding from the 

 subendothelial space of a rat 

 aorta. X 8,400. (Courtesy of 

 Robert M. O'Neal, Baylor 

 University.) 



