Hyperoxia prevents exercise-induced intrapulmonary arteriovenous shunt in healthy humans.

Department of Human Physiology, 1240 University of Oregon, Eugene, OR 97403-1240, USA.
The Journal of Physiology (Impact Factor: 4.38). 08/2008; 586(Pt 18):4559-65. DOI: 10.1113/jphysiol.2008.159350
Source: PubMed

ABSTRACT The 100% oxygen (O(2)) technique has been used to detect and quantify right-to-left shunt for more than 50 years. The goal of this study was to determine if breathing 100% O(2) affected intrapulmonary arteriovenous pathways during exercise. Seven healthy subjects (3 females) performed two exercise protocols. In Protocol I subjects performed an incremental cycle ergometer test (60 W + 30 W/2 min; breathing room air, FIO2 = 0.209) and arteriovenous shunting was evaluated using saline contrast echocardiography at each stage. Once significant arteriovenous shunting was documented (bubble score = 2), workload was held constant for the remainder of the protocol and FIO2 was alternated between 1.0 (hyperoxia) and 0.209 (normoxia) as follows: hyperoxia for 180 s, normoxia for 120 s, hyperoxia for 120 s, normoxia for 120 s, hyperoxia for 60 s and normoxia for 120 s. For Protocol II, subjects performed an incremental cycle ergometer test until volitional exhaustion while continuously breathing 100% O(2). In Protocol I, shunting was seen in all subjects at 120-300 W. Breathing oxygen for 1 min reduced shunting, and breathing oxygen for 2 min eliminated shunting in all subjects. Shunting promptly resumed upon breathing room air. Similarly, in Protocol II, breathing 100% O(2) substantially decreased or eliminated exercise-induced arteriovenous shunting in all subjects at submaximal and in 4/7 subjects at maximal exercise intensities. Our results suggest that alveolar hyperoxia prevents or reduces blood flow through arteriovenous shunt pathways.

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