Oxygen Transport and Smoking

Abstract

Many have considered the possibility that oxygen is a factor in the initiation of atherosclerosis, particularly hypoxia. An extensive review and resulting hypothesis of this phenomenon are presented by Hueper (1944), who suggested that hypoxic injury to the vascular wall occurs and increases the wall permeability. Robertson (1968) proposed a biochemical mechanism to describe hypoxia-induced atherosclerosis, in which it is assumed that hypoxia causes an increase in the permeability of the endothelial lining, after which cholesterol and lipids can diffuse into the intima and media. Hypoxia is also presumed to inhibit the ability of these cells to emulsify and disperse cytoplasmic lipids, and the lipid micelles are thus transformed into globular fat.