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Apnea causes microvascular perfusion maldistribution in isolated rat lungs
Obstructive sleep apnea is associated with significant cardiovascular disease, yet little is known about the effects of OSA on pulmonary microvascular perfusion. In a recent report, we showed that pulmonary microvascular perfusion was significantly mal‐distributed in anesthetized, spontaneously brea...
Autores principales: | , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
John Wiley and Sons Inc.
2019
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6499865/ https://www.ncbi.nlm.nih.gov/pubmed/31054186 http://dx.doi.org/10.14814/phy2.14085 |
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author | Conhaim, Robert L. Watson, Kal E. Broytman, Oleg Teodorescu, Mihaela |
author_facet | Conhaim, Robert L. Watson, Kal E. Broytman, Oleg Teodorescu, Mihaela |
author_sort | Conhaim, Robert L. |
collection | PubMed |
description | Obstructive sleep apnea is associated with significant cardiovascular disease, yet little is known about the effects of OSA on pulmonary microvascular perfusion. In a recent report, we showed that pulmonary microvascular perfusion was significantly mal‐distributed in anesthetized, spontaneously breathing rats exposed to five episodes of obstructive apnea. We quantified microvascular perfusion by analyzing trapping patterns of 4 μm diameter fluorescent latex particles infused into the pulmonary circulation after the last episode. We could not determine if the perfusion maldistribution was due to the effects of large subatmospheric intrapleural pressures during apnea, or to precapillary OSA hypoxic vasoconstriction. To address this, we repeated these studies using isolated, buffer‐perfused rat lungs (P (pulm art), 10 cm H(2)O) ventilated in a chamber (−5 to −15 cm H(2)O, 25 breaths/min; P (trachea) = 0). We simulated apnea by clamping the trachea and cycling the chamber pressures between −25 and −35 cm H(2)O for five breaths. After five apnea episodes, we infused 4 μm diam. fluorescent latex particles into the pulmonary artery. The number of particles recovered from the venous effluent was 74% greater in nonapneic isolated lungs compared to apneic lungs (P ≤ 0.05). Apneic lungs also had perfusion maldistributions that were 73% greater than those without apnea (P ≤ 0.05). We conclude that simulated apnea in isolated, perfused rat lungs produces significantly greater particle trapping and microvascular perfusion maldistribution than in nonapneic isolated lungs. We believe these effects are due to the large, negative intrapleural pressures produced during apnea, and are not due to hypoxia. |
format | Online Article Text |
id | pubmed-6499865 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2019 |
publisher | John Wiley and Sons Inc. |
record_format | MEDLINE/PubMed |
spelling | pubmed-64998652019-05-09 Apnea causes microvascular perfusion maldistribution in isolated rat lungs Conhaim, Robert L. Watson, Kal E. Broytman, Oleg Teodorescu, Mihaela Physiol Rep Original Research Obstructive sleep apnea is associated with significant cardiovascular disease, yet little is known about the effects of OSA on pulmonary microvascular perfusion. In a recent report, we showed that pulmonary microvascular perfusion was significantly mal‐distributed in anesthetized, spontaneously breathing rats exposed to five episodes of obstructive apnea. We quantified microvascular perfusion by analyzing trapping patterns of 4 μm diameter fluorescent latex particles infused into the pulmonary circulation after the last episode. We could not determine if the perfusion maldistribution was due to the effects of large subatmospheric intrapleural pressures during apnea, or to precapillary OSA hypoxic vasoconstriction. To address this, we repeated these studies using isolated, buffer‐perfused rat lungs (P (pulm art), 10 cm H(2)O) ventilated in a chamber (−5 to −15 cm H(2)O, 25 breaths/min; P (trachea) = 0). We simulated apnea by clamping the trachea and cycling the chamber pressures between −25 and −35 cm H(2)O for five breaths. After five apnea episodes, we infused 4 μm diam. fluorescent latex particles into the pulmonary artery. The number of particles recovered from the venous effluent was 74% greater in nonapneic isolated lungs compared to apneic lungs (P ≤ 0.05). Apneic lungs also had perfusion maldistributions that were 73% greater than those without apnea (P ≤ 0.05). We conclude that simulated apnea in isolated, perfused rat lungs produces significantly greater particle trapping and microvascular perfusion maldistribution than in nonapneic isolated lungs. We believe these effects are due to the large, negative intrapleural pressures produced during apnea, and are not due to hypoxia. John Wiley and Sons Inc. 2019-05-03 /pmc/articles/PMC6499865/ /pubmed/31054186 http://dx.doi.org/10.14814/phy2.14085 Text en Published 2019. This article is a U.S. Government work and is in the public domain in the USA. Physiological Reports published by Wiley Periodicals, Inc. on behalf of The Physiological Society and the American Physiological Society. This is an open access article under the terms of the http://creativecommons.org/licenses/by/4.0/ License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Original Research Conhaim, Robert L. Watson, Kal E. Broytman, Oleg Teodorescu, Mihaela Apnea causes microvascular perfusion maldistribution in isolated rat lungs |
title | Apnea causes microvascular perfusion maldistribution in isolated rat lungs |
title_full | Apnea causes microvascular perfusion maldistribution in isolated rat lungs |
title_fullStr | Apnea causes microvascular perfusion maldistribution in isolated rat lungs |
title_full_unstemmed | Apnea causes microvascular perfusion maldistribution in isolated rat lungs |
title_short | Apnea causes microvascular perfusion maldistribution in isolated rat lungs |
title_sort | apnea causes microvascular perfusion maldistribution in isolated rat lungs |
topic | Original Research |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6499865/ https://www.ncbi.nlm.nih.gov/pubmed/31054186 http://dx.doi.org/10.14814/phy2.14085 |
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