Abstract
The compressed gas breath during diving augments partial pressure of oxygen causing the oxygen concentration of the blood to increase above normal (hyperoxia). Hyperoxia in combination with gas bubbles that develop during the decompression (ascent) phase, likely causing oxidative stress, including transient endothelial dysfunction in venous and arterial vessels. The number of aging divers is rising and aging itself is associated with a gradual impairment of endothelial function. These alterations play a central role in the pathogenesis of atherosclerosis and coronary artery disease. While diving and aging are independent modulators of cardiovascular function, little is known about their combined effect. Thus, the central question is does diving expose old divers to more oxidative stress or not?MethodApoE homozygous knockouts rats with impaired cardiovascular function were used as a model for aging. 10 ApoE rats (male and female) exposed to 500 kPa heliox gas (80% helium/20% oxygen) for 1 hr in a pressure chamber to simulate diving. Endothelial function examined in‐vitro by myograph in pulmonary and mesenteric artery. The oxidative stress biomarkers measured in the plasma (collected from heart) and lung tissue via TBARS assay. 10 ApoE rats served as a control group.Results and conclusionThe results of this study demonstrated that a single dive causes endothelial dysfunction in pulmonary arteries of rats with aging cardiovascular system. This seems to be caused by reduction in NO synthesis (Fig. 1). These responses were observed just in male rats.Support or Funding InformationThis project was funded by Aarhus University.This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.
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