Vascular Wall PO₂ Following Carbon Monoxide Exposure

Abstract

Cigarette smoking and atherosclerosis may be linked to vascular wall damage caused by carbon monoxide (CO), nocotine or exposure to other toxic substances. Vascular wall hypoxia may play an important role in this process. Schneiderman and Goldstick (1,2) have simulated the effect of CO exposure on O₂ transport to the wall of the human thoracic aorta using a computer model. The wall of the thoracic aorta and other large blood vessels must depend on O₂ supply from both the vessel lumen and from the microvasculature of the outer wall (vasa vasorum). A two layer tissue model was chosen to represent the vascular wall in their analysis, with the tissue properties (O₂consumption rate, Q, diffusivity, D, and solubility, K) for each layer estimated from the literature. The location and value of the minimum PO₂ (P_min) in the wall will depend on these tissue properties, as well as the wall dimensions and boundary conditions at the inner endothelial and outer adventitial edges of the a vascular portion of the wall. The computer studies indicate that P_min will decrease with increasing levels of carboxyhemoglobin (COHb) within the range experienced by heavy smokers (up to 20%). Their model predicts that the middle or inner medial layer is most susceptible to hypoxic damage.