Atherosclerosis and Alimentary Hyperlipemia

Abstract

It was found that 3-5 hrs. after a fatty meal, the physical state of the lipid particles in the plasma was qualitatively the same as in sustained hyperlipemia. This change in physical state consisted of markedly greater numbers of lipid particles of much larger size than those occurring in normal fasting plasma or after fat-free meals. The physical state and particle size of the plasma lipids were studied by: (1) direct observation and photomicrography of high-power, darkfield prepns.; (2) Tyndall effect and nephelometry; and (3) high-speed centrifugation. The theory is proposed that the cumulative effect of many fatty meals in a lifetime, by producing the transient showers of large lipid particles in the plasma, may be the basic cause of the intimal lipid deposition in atherosclerosis. The deposition occurs primarily in the tissue spaces of the arterial intima between the overlying en-dothelium and the underlying barrier of the fenestrated internal elastic membrane. The particles are retained and deposited from the lymph stream which passes from the lumen through the intramural structures toward the adventitial venules and lymphatics. The increased particle size of the lipids in sustained or alimentary hyperlipemia stimulates phagocytosis in the intima by macrophages and formation of "foam cells". The barrier function of the fenestrated or even reduplicated internal elastic membrane may be important in the mechanics of lipid-particle retention in the intimal tissue spaces. The neutral fats and fatty acids in the depositing lipid particles are more readily resorbed and removed than cholesterol and cholesterol esters. The evidence in support of the chylomicron theory is given.