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• W4243153217 abstract "POINT-COUNTERPOINTRebuttal from Hopkins, Olfert, and WagnerPublished Online:01 Sep 2009https://doi.org/10.1152/japplphysiol.91489.2008bMoreSectionsPDF (49 KB)Download PDF ToolsExport citationAdd to favoritesGet permissionsTrack citations ShareShare onFacebookTwitterLinkedInWeChat Our colleagues suggest that transpulmonary microbubble passage demonstrates shunting important for gas exchange during exercise (5). However, they themselves show that flow through vessels allowing 25 μm microsphere transmission is generally very small and have never demonstrated any associated gas exchange effect. They are trying to elevate the status of miniscule arteriovenous pathways into elephant-sized shunts.They demonstrate microsphere transmission of only 0.001–0.05% of cardiac output at resting flows (6, 8), less than the small ∼0.2% found with the multiple inert gas technique (MIGET). During exercise, MIGET-detected shunt in humans (3) and dogs (4) averages 0.1%. In exercising dogs (8), our colleagues report pulmonary microsphere transmission of 1.42%, which they interpret as a 1.42% shunt. In pulmonary gas exchange, shunt has only one definition—blood not exposed to ventilated alveoli during passage through the lungs. Shunted blood does not participate in gas exchange and arterial PO2 thus falls. Importantly in their dogs, PaO2 increased with exercise (from 99 to 106 Torr) while estimated AaDO2 was unchanged at 10 Torr. First, PaO2 increasing to 106 Torr contradicts the assertion that “shunts” are important during exercise. Second, a 10 Torr AaDO2 is entirely accounted for by a shunt of at most 0.6%. Thus the majority of the 1.42% flow indicated by microspheres cannot be a shunt. Third, if shunts appear only during exercise, why didn't the AaDO2 increase during exercise?Our colleagues find that microbubble transmission correlates with the AaDO2 during exercise (9), but many variables correlate without any cause-and-effect relationship. They also argue that precapillary gas exchange impairs the ability of MIGET to detect shunts, as low-solubility gases are eliminated upstream of shunt vessels. However, where pathologic intrapulmonary shunt and hypoxemia are expected (e.g., hepatopulmonary syndrome, pulmonary edema), shunt is readily detected with MIGET (1, 7). Also, since precapillary gas exchange has been shown for oxygen in normal lungs (2), their explanation is unlikely, as it should similarly overcome “shunting” for O2 if such occurred in the arteriovenous pathways found by our colleagues.Finally, they suggest that using 100% oxygen for measuring shunt is invalid, implying that O2 constricts some of the pulmonary circulation (5). However what they demonstrate is the disappearance of microbubbles, not of shunt. There are several explanations for this that do not involve rewriting the textbooks on the effects of oxygen on the pulmonary circulation, including how changing gas partial pressures affect microbubble size (10).REFERENCES1 Castaing Y, Manier G. Hemodynamic disturbances and VA/Q matching in hypoxemic cirrhotic patients. Chest 96: 1064–1069, 1989.Crossref | ISI | Google Scholar2 Conhaim RL, Staub NC. Reflection spectrophotometric measurement of O2 uptake in pulmonary arterioles of cats. J Appl Physiol 48: 848–856, 1980.Link | ISI | Google Scholar3 Hopkins SR, Olfert IM, Wagner PD. Point: exercise-induced intrapulmonary shunting is imaginary. J Appl Physiol; doi:10.1152/japplphysiol.91489.2008.Link | ISI | Google Scholar4 Hsia CC, Johnson RL Jr, McDonough P, Dane DM, Hurst MD, Fehmel JL, Wagner HE, Wagner PD. Residence at 3,800-m altitude for 5 mo in growing dogs enhances lung diffusing capacity for oxygen that persists at least 25 years. J Appl Physiol 102: 1448–1455, 2007.Link | ISI | Google Scholar5 Lovering AT, Eldridge MW, Stickland MK. Counterpoint: exercise-induced intrapulmonary shunting is real. J Appl Physiol; doi:10.1152/japplphysiol.91489.2008a.Link | ISI | Google Scholar6 Lovering AT, Stickland MK, Kelso AJ, Eldridge MW. Direct demonstration of 25- and 50-μm arteriovenous pathways in healthy human and baboon lungs. Am J Physiol Heart Circ Physiol 292: H1777–H1781, 2007.Link | ISI | Google Scholar7 Reyes A, Roca J, Rodriguez-Roisin R, Torres A, Ussetti P, Wagner PD. Effect of almitrine on ventilation-perfusion distribution in adult respiratory distress syndrome. Am Rev Respir Dis 137: 1062–1067, 1988.Crossref | PubMed | ISI | Google Scholar8 Stickland MK, Lovering AT, Eldridge MW. Exercise-induced arteriovenous intrapulmonary shunting in dogs. Am J Respir Crit Care Med 176: 300–305, 2007.Crossref | ISI | Google Scholar9 Stickland MK, Welsh RC, Haykowsky MJ, Petersen SR, Anderson WD, Taylor DA, Bouffard M, Jones RL. Intra-pulmonary shunt and pulmonary gas exchange during exercise in humans. J Physiol 561: 321–329, 2004.Crossref | PubMed | ISI | Google Scholar10 Van Liew HD, Burkard ME. Bubbles in circulating blood: stabilization and simulations of cyclic changes of size and content. J Appl Physiol 79: 1379–1385, 1995.Link | ISI | Google Scholar Download PDF Previous Back to Top Next FiguresReferencesRelatedInformation Cited ByA case of intrapulmonary transmission of air while transitioning a patient from a sitting to a supine position after venous air embolism during a craniotomy2 March 2012 | Canadian Journal of Anesthesia/Journal canadien d'anesthésie, Vol. 59, No. 5Sonic echocardiography: what does it mean when there are no bubbles in the left ventricle?Hugh D. Van Liew, and Richard D. Vann1 January 2011 | Journal of Applied Physiology, Vol. 110, No. 1Hypoxia-induced intrapulmonary arteriovenous shunting at rest in healthy humansSteven S. Laurie, Ximeng Yang, Jonathan E. Elliott, Kara M. Beasley, and Andrew T. Lovering1 October 2010 | Journal of Applied Physiology, Vol. 109, No. 4 More from this issue > Volume 107Issue 3September 2009Pages 997-998 Copyright & PermissionsCopyright © 2009 the American Physiological Societyhttps://doi.org/10.1152/japplphysiol.91489.2008bHistory Published online 1 September 2009 Published in print 1 September 2009 Metrics" @default.
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