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Vascular Wall PO2 Following Carbon Monoxide Exposure

  • Donald G. Buerk
  • Thomas K. Goldstick
Part of the Advances in Experimental Medicine and Biology book series (AEMB, volume 159)

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 (Pmin) 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 Pmin 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.

Keywords

Thoracic Aorta Vascular Wall Outer Wall Vessel Lumen Hypoxic Damage 
These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.

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Copyright information

© Plenum Press, New York 1983

Authors and Affiliations

  • Donald G. Buerk
    • 1
  • Thomas K. Goldstick
    • 1
  1. 1.Department of Chemical EngineeringNorthwestern UniversityEvanstonUSA

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