Elevated pulmonary artery pressure and brain natriuretic peptide in high altitude pulmonary edema susceptible non-mountaineers

Exaggerated pulmonary pressor response to hypoxia is a pathgonomic feature observed in high altitude pulmonary edema (HAPE) susceptible mountaineers. It was investigated whether measurement of basal pulmonary artery pressure (Ppa) and brain natriuretic peptide (BNP) could improve identification of H...

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Veröffentlicht in:Scientific reports 2016-02, Vol.6 (1), p.21357-21357, Article 21357
Hauptverfasser: Gupta, Rajinder K., Himashree, G., Singh, Krishan, Soree, Poonam, Desiraju, Koundinya, Agrawal, Anurag, Ghosh, Dishari, Dass, Deepak, Reddy, Prassana K., Panjwani, Usha, Singh, Shashi Bala
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container_title Scientific reports
container_volume 6
creator Gupta, Rajinder K.
Himashree, G.
Singh, Krishan
Soree, Poonam
Desiraju, Koundinya
Agrawal, Anurag
Ghosh, Dishari
Dass, Deepak
Reddy, Prassana K.
Panjwani, Usha
Singh, Shashi Bala
description Exaggerated pulmonary pressor response to hypoxia is a pathgonomic feature observed in high altitude pulmonary edema (HAPE) susceptible mountaineers. It was investigated whether measurement of basal pulmonary artery pressure (Ppa) and brain natriuretic peptide (BNP) could improve identification of HAPE susceptible subjects in a non-mountaineer population. We studied BNP levels, baseline hemodynamics and the response to hypoxia (FIo 2  = 0.12 for 30 min duration at sea level) in 11 HAPE resistant (no past history of HAPE, Control) and 11 HAPE susceptible (past history of HAPE, HAPE-S) subjects. Baseline Ppa (19.31 ± 3.63 vs 15.68 ± 2.79 mm Hg, p 
doi_str_mv 10.1038/srep21357
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It was investigated whether measurement of basal pulmonary artery pressure (Ppa) and brain natriuretic peptide (BNP) could improve identification of HAPE susceptible subjects in a non-mountaineer population. We studied BNP levels, baseline hemodynamics and the response to hypoxia (FIo 2  = 0.12 for 30 min duration at sea level) in 11 HAPE resistant (no past history of HAPE, Control) and 11 HAPE susceptible (past history of HAPE, HAPE-S) subjects. Baseline Ppa (19.31 ± 3.63 vs 15.68 ± 2.79 mm Hg, p < 0.05) and plasma BNP levels (52.39 ± 32.9 vs 15.05 ± 9.6 pg/ml, p < 0.05) were high and stroke volume was less (p < 0.05) in HAPE-S subjects compared to control. Acute hypoxia produced an exaggerated increase in heart rate (p < 0.05), mean arterial pressure (p < 0.05) and Ppa (28.2 ± 5.8 vs 19.33 ± 3.74 mm Hg, p < 0.05) and fall in peripheral oxygen saturation (p < 0.05) in HAPE-S compared to control. Receiver operating characteristic (ROC) curves showed that Ppa response to acute hypoxia was the best variable to identify HAPE susceptibility (AUC 0.92) but BNP levels provided comparable information (AUC 0.85). BNP levels are easy to determine and may represent an important marker for the determination of HAPE susceptibility.]]></description><identifier>ISSN: 2045-2322</identifier><identifier>EISSN: 2045-2322</identifier><identifier>DOI: 10.1038/srep21357</identifier><identifier>PMID: 26892302</identifier><language>eng</language><publisher>London: Nature Publishing Group UK</publisher><subject>692/499 ; 692/699/1785/3193 ; 692/699/75/593 ; Adult ; Altitude ; Altitude Sickness - metabolism ; Altitude Sickness - physiopathology ; Anthropometry ; Blood Pressure ; Brain natriuretic peptide ; Case-Control Studies ; Disease Susceptibility ; Edema ; Heart rate ; Hemodynamics ; High-altitude environments ; Humanities and Social Sciences ; Humans ; Hypertension, Pulmonary - metabolism ; Hypertension, Pulmonary - physiopathology ; Hypoxia ; Hypoxia - metabolism ; Hypoxia - physiopathology ; multidisciplinary ; Natriuretic Peptide, Brain - metabolism ; Population studies ; Pulmonary arteries ; Pulmonary artery ; Pulmonary Artery - physiopathology ; Respiratory Function Tests ; Science ; Stroke</subject><ispartof>Scientific reports, 2016-02, Vol.6 (1), p.21357-21357, Article 21357</ispartof><rights>The Author(s) 2016</rights><rights>Copyright Nature Publishing Group Feb 2016</rights><rights>Copyright © 2016, Macmillan Publishers Limited 2016 Macmillan Publishers Limited</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c438t-1e0c3fba521090781707f96cb3b23e5114bec5d6f26510635559fea37872ed223</citedby><cites>FETCH-LOGICAL-c438t-1e0c3fba521090781707f96cb3b23e5114bec5d6f26510635559fea37872ed223</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC4759542/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC4759542/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,864,885,27924,27925,41120,42189,51576,53791,53793</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/26892302$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Gupta, Rajinder K.</creatorcontrib><creatorcontrib>Himashree, G.</creatorcontrib><creatorcontrib>Singh, Krishan</creatorcontrib><creatorcontrib>Soree, Poonam</creatorcontrib><creatorcontrib>Desiraju, Koundinya</creatorcontrib><creatorcontrib>Agrawal, Anurag</creatorcontrib><creatorcontrib>Ghosh, Dishari</creatorcontrib><creatorcontrib>Dass, Deepak</creatorcontrib><creatorcontrib>Reddy, Prassana K.</creatorcontrib><creatorcontrib>Panjwani, Usha</creatorcontrib><creatorcontrib>Singh, Shashi Bala</creatorcontrib><title>Elevated pulmonary artery pressure and brain natriuretic peptide in high altitude pulmonary edema susceptible non-mountaineers</title><title>Scientific reports</title><addtitle>Sci Rep</addtitle><addtitle>Sci Rep</addtitle><description><![CDATA[Exaggerated pulmonary pressor response to hypoxia is a pathgonomic feature observed in high altitude pulmonary edema (HAPE) susceptible mountaineers. It was investigated whether measurement of basal pulmonary artery pressure (Ppa) and brain natriuretic peptide (BNP) could improve identification of HAPE susceptible subjects in a non-mountaineer population. We studied BNP levels, baseline hemodynamics and the response to hypoxia (FIo 2  = 0.12 for 30 min duration at sea level) in 11 HAPE resistant (no past history of HAPE, Control) and 11 HAPE susceptible (past history of HAPE, HAPE-S) subjects. Baseline Ppa (19.31 ± 3.63 vs 15.68 ± 2.79 mm Hg, p < 0.05) and plasma BNP levels (52.39 ± 32.9 vs 15.05 ± 9.6 pg/ml, p < 0.05) were high and stroke volume was less (p < 0.05) in HAPE-S subjects compared to control. Acute hypoxia produced an exaggerated increase in heart rate (p < 0.05), mean arterial pressure (p < 0.05) and Ppa (28.2 ± 5.8 vs 19.33 ± 3.74 mm Hg, p < 0.05) and fall in peripheral oxygen saturation (p < 0.05) in HAPE-S compared to control. Receiver operating characteristic (ROC) curves showed that Ppa response to acute hypoxia was the best variable to identify HAPE susceptibility (AUC 0.92) but BNP levels provided comparable information (AUC 0.85). BNP levels are easy to determine and may represent an important marker for the determination of HAPE susceptibility.]]></description><subject>692/499</subject><subject>692/699/1785/3193</subject><subject>692/699/75/593</subject><subject>Adult</subject><subject>Altitude</subject><subject>Altitude Sickness - metabolism</subject><subject>Altitude Sickness - physiopathology</subject><subject>Anthropometry</subject><subject>Blood Pressure</subject><subject>Brain natriuretic peptide</subject><subject>Case-Control Studies</subject><subject>Disease Susceptibility</subject><subject>Edema</subject><subject>Heart rate</subject><subject>Hemodynamics</subject><subject>High-altitude environments</subject><subject>Humanities and Social Sciences</subject><subject>Humans</subject><subject>Hypertension, Pulmonary - metabolism</subject><subject>Hypertension, Pulmonary - physiopathology</subject><subject>Hypoxia</subject><subject>Hypoxia - metabolism</subject><subject>Hypoxia - physiopathology</subject><subject>multidisciplinary</subject><subject>Natriuretic Peptide, Brain - metabolism</subject><subject>Population studies</subject><subject>Pulmonary arteries</subject><subject>Pulmonary artery</subject><subject>Pulmonary Artery - physiopathology</subject><subject>Respiratory Function Tests</subject><subject>Science</subject><subject>Stroke</subject><issn>2045-2322</issn><issn>2045-2322</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2016</creationdate><recordtype>article</recordtype><sourceid>C6C</sourceid><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><recordid>eNplkU1r3DAQhkVoSUKaQ_9AEPTSBpzqw7KsSyGEpC0EcknPQrbHuwq25OgjkEt-e7Vsut02uoyYeXjnHV6EPlJyQQlvv8YAC6NcyAN0zEgtKsYZe7f3P0KnMT6Q8gRTNVWH6Ig1rWKcsGP0cj3Bk0kw4CVPs3cmPGMTEpSyBIgxB8DGDbgLxjrsTAq2tJLt8QJLsgPg0l7b1RqbKdmUS-OvEAwwGxxz7DdsNwF23lWzzy4VNYAQP6D3o5kinL7WE_Tr5vr-6kd1e_f959XlbdXXvE0VBdLzsTOCUaKIbKkkclRN3_GOcRCU1h30YmhG1ghKGi6EUCMYLlvJYGCMn6BvW90ldzMMPbgUzKSXYOdiVHtj9b8TZ9d65Z90LYUS9Ubg86tA8I8ZYtKzLWdNk3Hgc9RUNsWTbOq6oJ_-Qx98Dq6cp2mrWtVwLjaCX7ZUH3wsGY47M5ToTbB6F2xhz_bd78g_MRbgfAvEMnIrCHsr36j9Botwr8Q</recordid><startdate>20160219</startdate><enddate>20160219</enddate><creator>Gupta, Rajinder K.</creator><creator>Himashree, G.</creator><creator>Singh, Krishan</creator><creator>Soree, Poonam</creator><creator>Desiraju, Koundinya</creator><creator>Agrawal, Anurag</creator><creator>Ghosh, Dishari</creator><creator>Dass, Deepak</creator><creator>Reddy, Prassana K.</creator><creator>Panjwani, Usha</creator><creator>Singh, Shashi Bala</creator><general>Nature Publishing Group UK</general><general>Nature Publishing Group</general><scope>C6C</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7X7</scope><scope>7XB</scope><scope>88A</scope><scope>88E</scope><scope>88I</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AEUYN</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M2P</scope><scope>M7P</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>Q9U</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>20160219</creationdate><title>Elevated pulmonary artery pressure and brain natriuretic peptide in high altitude pulmonary edema susceptible non-mountaineers</title><author>Gupta, Rajinder K. ; 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It was investigated whether measurement of basal pulmonary artery pressure (Ppa) and brain natriuretic peptide (BNP) could improve identification of HAPE susceptible subjects in a non-mountaineer population. We studied BNP levels, baseline hemodynamics and the response to hypoxia (FIo 2  = 0.12 for 30 min duration at sea level) in 11 HAPE resistant (no past history of HAPE, Control) and 11 HAPE susceptible (past history of HAPE, HAPE-S) subjects. Baseline Ppa (19.31 ± 3.63 vs 15.68 ± 2.79 mm Hg, p < 0.05) and plasma BNP levels (52.39 ± 32.9 vs 15.05 ± 9.6 pg/ml, p < 0.05) were high and stroke volume was less (p < 0.05) in HAPE-S subjects compared to control. Acute hypoxia produced an exaggerated increase in heart rate (p < 0.05), mean arterial pressure (p < 0.05) and Ppa (28.2 ± 5.8 vs 19.33 ± 3.74 mm Hg, p < 0.05) and fall in peripheral oxygen saturation (p < 0.05) in HAPE-S compared to control. Receiver operating characteristic (ROC) curves showed that Ppa response to acute hypoxia was the best variable to identify HAPE susceptibility (AUC 0.92) but BNP levels provided comparable information (AUC 0.85). BNP levels are easy to determine and may represent an important marker for the determination of HAPE susceptibility.]]></abstract><cop>London</cop><pub>Nature Publishing Group UK</pub><pmid>26892302</pmid><doi>10.1038/srep21357</doi><tpages>1</tpages><oa>free_for_read</oa></addata></record>
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subjects 692/499
692/699/1785/3193
692/699/75/593
Adult
Altitude
Altitude Sickness - metabolism
Altitude Sickness - physiopathology
Anthropometry
Blood Pressure
Brain natriuretic peptide
Case-Control Studies
Disease Susceptibility
Edema
Heart rate
Hemodynamics
High-altitude environments
Humanities and Social Sciences
Humans
Hypertension, Pulmonary - metabolism
Hypertension, Pulmonary - physiopathology
Hypoxia
Hypoxia - metabolism
Hypoxia - physiopathology
multidisciplinary
Natriuretic Peptide, Brain - metabolism
Population studies
Pulmonary arteries
Pulmonary artery
Pulmonary Artery - physiopathology
Respiratory Function Tests
Science
Stroke
title Elevated pulmonary artery pressure and brain natriuretic peptide in high altitude pulmonary edema susceptible non-mountaineers
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