Hyperoxia prevents exercise-induced intrapulmonary arteriovenous shunt in healthy humans
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 pr...
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Veröffentlicht in: | The Journal of physiology 2008-09, Vol.586 (18), p.4559-4565 |
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Zusammenfassung: | 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, ) 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 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 120â300 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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ISSN: | 0022-3751 1469-7793 |
DOI: | 10.1113/jphysiol.2008.159350 |