{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,8]],"date-time":"2026-09-08T12:35:06Z","timestamp":1788870906242,"version":"build-2803163510"},"reference-count":56,"publisher":"Wiley","issue":"3","license":[{"start":{"date-parts":[[2014,12,23]],"date-time":"2014-12-23T00:00:00Z","timestamp":1419292800000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"funder":[{"name":"Natural Sciences and Engineering Research Council of Canada (NSERC)"},{"name":"Canadian Foundation for Innovation (CFI)"},{"name":"Canadian Institutes of Health Research (CIHR)"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["The Journal of Physiology"],"published-print":{"date-parts":[[2015,2]]},"abstract":"\n Key points<\/jats:title>\n \n \n \n Blood flow through intrapulmonary arteriovenous anastomoses (IPAVA) is increased by acute hypoxia during rest by unknown mechanisms.<\/jats:p>\n <\/jats:list-item>\n \n Oral administration of acetazolamide blunts the pulmonary vascular pressure response to acute hypoxia, thus permitting the observation of IPAVA blood flow with minimal pulmonary pressure change.<\/jats:p>\n <\/jats:list-item>\n \n \n Hypoxic pulmonary vasoconstriction was attenuated in humans following acetazolamide administration and partially restored with bicarbonate infusion, indicating that the effects of acetazolamide on hypoxic pulmonary vasoconstriction may involve an interaction between arterial pH and\n \n .\n <\/jats:p>\n <\/jats:list-item>\n \n \n We observed that IPAVA blood flow during hypoxia was similar before and after acetazolamide administration, even after acid\u2013base status correction, indicating that pulmonary pressure, pH and\n \n are unlikely regulators of IPAVA blood flow.\n <\/jats:p>\n <\/jats:list-item>\n <\/jats:list>\n <\/jats:p>\n <\/jats:sec>\n \n Abstract<\/jats:title>\n \n Blood flow through intrapulmonary arteriovenous anastomoses (IPAVA) is increased with exposure to acute hypoxia and has been associated with pulmonary artery systolic pressure (PASP). We aimed to determine the direct relationship between blood flow through IPAVA and PASP in 10 participants with no detectable intracardiac shunt by comparing: (1) isocapnic hypoxia (control); (2) isocapnic hypoxia with oral administration of acetazolamide (AZ; 250\u00a0mg, three times a day for 48\u00a0h) to prevent increases in PASP; and (3) isocapnic hypoxia with AZ and 8.4% NaHCO\n 3<\/jats:sub>\n infusion (AZ\u00a0+\u00a0HCO\n 3<\/jats:sub>\n \u2013<\/jats:sup>\n ) to control for AZ\u2010induced acidosis. Isocapnic hypoxia (20\u00a0min) was maintained by end\u2010tidal forcing, blood flow through IPAVA was determined by agitated saline contrast echocardiography and PASP was estimated by Doppler ultrasound. Arterial blood samples were collected at rest before each isocapnic\u2013hypoxia condition to determine pH, [HCO\n 3<\/jats:sub>\n \u2013<\/jats:sup>\n ] and\n \n . AZ decreased pH (\u20130.08\u00a0\u00b1\u00a00.01), [HCO\n 3<\/jats:sub>\n \u2013<\/jats:sup>\n ] (\u22127.1\u00a0\u00b1\u00a00.7\u00a0mmol\u00a0l\n \u22121<\/jats:sup>\n ) and\n \n (\u22124.5\u00a0\u00b1\u00a01.4\u00a0mmHg;\n P<\/jats:italic>\n \u00a0<\u00a00.01), while intravenous NaHCO\n 3<\/jats:sub>\n restored arterial blood gas parameters to control levels. Although PASP increased from baseline in all three hypoxic conditions (\n P<\/jats:italic>\n \u00a0<\u00a00.05), a main effect of condition expressed an 11\u00a0\u00b1\u00a02% reduction in PASP from control (\n P<\/jats:italic>\n \u00a0<\u00a00.001) following AZ administration while intravenous NaHCO\n 3<\/jats:sub>\n partially restored the PASP response to isocapnic hypoxia. Blood flow through IPAVA increased during exposure to isocapnic hypoxia (\n P<\/jats:italic>\n \u00a0<\u00a00.01) and was unrelated to PASP, cardiac output and pulmonary vascular resistance for all conditions. In conclusion, isocapnic hypoxia induces blood flow through IPAVA independent of changes in PASP and the influence of AZ on the PASP response to isocapnic hypoxia is dependent upon the H\n +<\/jats:sup>\n concentration or\n \n .\n <\/jats:p>\n <\/jats:sec>","DOI":"10.1113\/jphysiol.2014.282962","type":"journal-article","created":{"date-parts":[[2014,11,22]],"date-time":"2014-11-22T00:10:06Z","timestamp":1416615006000},"page":"723-737","source":"Crossref","is-referenced-by-count":31,"title":["Hypoxia, not pulmonary vascular pressure, induces blood flow through intrapulmonary arteriovenous anastomoses"],"prefix":"10.1113","volume":"593","author":[{"given":"Joshua C.","family":"Tremblay","sequence":"first","affiliation":[{"name":"Centre for Heart Lung and Vascular Health School of Health and Exercise Science University of British Columbia Kelowna BC Canada"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Andrew T.","family":"Lovering","sequence":"additional","affiliation":[{"name":"Department of Human Physiology University of Oregon Eugene OR USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Philip N.","family":"Ainslie","sequence":"additional","affiliation":[{"name":"Centre for Heart Lung and Vascular Health School of Health and Exercise Science University of British Columbia Kelowna BC Canada"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Mike","family":"Stembridge","sequence":"additional","affiliation":[{"name":"Cardiff School of Sport Cardiff Metropolitan University Cardiff UK"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Keith R.","family":"Burgess","sequence":"additional","affiliation":[{"name":"Department of Medicine University of Sydney Sydney NSW Australia"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Akke","family":"Bakker","sequence":"additional","affiliation":[{"name":"MIRA Institute University of Twente Enschede Netherlands"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Joseph","family":"Donnelly","sequence":"additional","affiliation":[{"name":"Division of Neurosurgery Department of Clinical Neurosciences University of Cambridge UK"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Samuel J.E.","family":"Lucas","sequence":"additional","affiliation":[{"name":"School of Sport Exercise and Rehabilitation Sciences University of Birmingham Birmingham UK"},{"name":"Department of Physiology & School of Physical Education and Exercise Sciences University of Otago New Zealand"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Nia C.S.","family":"Lewis","sequence":"additional","affiliation":[{"name":"Centre for Heart Lung and Vascular Health School of Health and Exercise Science University of British Columbia Kelowna BC Canada"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Paolo B.","family":"Dominelli","sequence":"additional","affiliation":[{"name":"School of Kinesiology University of British Columbia Vancouver BC Canada"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"William R.","family":"Henderson","sequence":"additional","affiliation":[{"name":"School of Kinesiology University of British Columbia Vancouver BC Canada"},{"name":"Division of Critical Care Medicine Department of Medicine Faculty of Medicine University of British Columbia Vancouver BC Canada"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Giulio S.","family":"Dominelli","sequence":"additional","affiliation":[{"name":"Division of Respirology Faculty of Medicine University of British Columbia Vancouver BC Canada"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"A. 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