Increases in coronary vascular resistance related to high arterial oxygen tension in dogs.

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Abstract
O2 inhalation induces coronary vessel constriction and causes a reduction in myocardial O2 consumption. Whether or not this constriction of the coronary vessels resulting from O2 is secondary to the reduction in myocardial O2 consumption is studied. The regional myocardium in 12 mongrel dogs was perfused with femoral arterial blood at a constant rate of flow. While maintaining myocardial O2 consumption equal by adjusting heart rate, coronary vascular resistance was compared under the 2 following conditions: perfusion of the coronary artery with the dog''s own femoral arterial blood (pO2 [partial pressure of O2]: 95 .+-. 14 mm Hg) and perfusion with blood with a high level of O2 tension (pO2: 497 .+-. 56 mm Hg). Coronary vascular resistance was increased (P < 0.001) from 3.00 .+-. 1.25 to 3.36 .+-. 1.28 mm Hg/ml per min by increasing the pO2 in the perfusing blood, even though myocardial O2 consumption was kept at the same level. This increase in coronary vascular resistance resulting from the increase in O2 tension was independent of the coronary perfusion rate and independent of the presence or absence of myocardial ischemia. Coronary vasoconstriction due to O2 apparently is not secondary to decreases in myocardial O2 demand.

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