Intrapulmonary arteriovenous shunts of 15 m in diameter probably do not contribute to arterial hypoxemia in maximally exercising Thoroughbred horses

Manohar, Murli, and Thomas E. Goetz. Intrapulmonary arteriovenous shunts of 15 m in diameter probably do not contribute to arterial hypoxemia in maximally exercising Thoroughbred horses. J Appl Physiol 99: 224–229, 2005. First published March 17, 2005; doi:10.1152/japplphysiol.01230.2004.—The present study examined whether Thoroughbred horses performing strenuous exercise exhibit intrapulmonary arteriovenous shunting that may contribute to the observed arterial hypoxemia. Experiments were carried out on seven healthy, exercise-trained Thoroughbreds at rest, maximal exercise (galloping at 14 m/s on a 3.5% uphill grade for 120 s), and submaximal exertion (8 m/s on a 3.5% uphill grade for 150 s). Along with blood gas/hemodynamic parameters, intrapulmonary arteriovenous shunting was studied by injecting 15m-diameter microspheres, labeled with different stable isotopes, into the right atrium while simultaneous blood samples were being withdrawn at a constant rate from the pulmonary artery and the aorta. Arterial hypoxemia was observed only during maximal exercise. Also, despite significant pulmonary arterial hypertension during submaximal and maximal exertion, 15m microspheres did not traverse the pulmonary microcirculation to appear in the aortic blood. Thus our findings did not support a role for intrapulmonary arteriovenous shunts of 15 m in diameter in the exercise-induced arterial hypoxemia in racehorses. Interestingly, our observation that, in going from 30 to 120 s of maximal exertion, arterial O2 tension had remained unchanged despite significant reductions in mixed venous blood O2 tension, hemoglobin-O2 saturation, and O2 content also discounts the importance of intrapulmonary arteriovenous shunts in causing arterial hypoxemia. This is because, assuming that a constant fraction of total pulmonary blood flow bypasses the gas-exchange areas of the equine lungs via intrapulmonary arteriovenous shunts during 30–120 s of maximal exertion, the observed significant reductions in mixed venous blood oxygenation should cause a significant reduction in arterial O2 tension, which was not the case in our horses. Thus it is suggested that intrapulmonary arteriovenous shunting probably does not contribute to the exercise-induced arterial hypoxemia in racehorses.