Hypoxia Impairs Systemic Endothelial Function in Individuals Prone to High-Altitude Pulmonary Edema
High-altitude pulmonary edema (HAPE) is characterized by excessive pulmonary vasoconstriction and is associated with decreased concentrations of nitric oxide (NO) in the lung. We hypothesized that individuals susceptible to HAPE (HAPE-S) would also have dysfunction of the vascular NO vasodilator pat...
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| Veröffentlicht in: | American journal of respiratory and critical care medicine 2005-09, Vol.172 (6), p.763-767 |
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| container_title | American journal of respiratory and critical care medicine |
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| creator | Berger, Marc M Hesse, Christiane Dehnert, Christoph Siedler, Heike Kleinbongard, Petra Bardenheuer, Hubert J Kelm, Malte Bartsch, Peter Haefeli, Walter E |
| description | High-altitude pulmonary edema (HAPE) is characterized by excessive pulmonary vasoconstriction and is associated with decreased concentrations of nitric oxide (NO) in the lung.
We hypothesized that individuals susceptible to HAPE (HAPE-S) would also have dysfunction of the vascular NO vasodilator pathway during hypoxia in the systemic vasculature.
During normoxia (FI(O(2)) = 0.21) and 4 hours of normobaric hypoxia (FI(O(2)) = 0.12, corresponding to an altitude of 4,500 m above sea level) endothelium-dependent and endothelium-independent vasodilator responses to intraarterial infusion of acetylcholine (ACh) and sodium nitroprusside, respectively, were measured by forearm venous occlusion plethysmography in nine HAPE-S subjects and in nine HAPE-resistant control subjects.
Pulmonary artery systolic pressure increased from 22 +/- 3 to 33 +/- 6 mm Hg (p < 0.001) during hypoxia in control subjects, and from 25 +/- 4 to 50 +/- 9 mm Hg in HAPE-S subjects (p < 0.001). Despite similar responses during normoxia in both groups, ACh-induced changes in forearm blood flow markedly decreased during hypoxia in HAPE-S subjects (p = 0.01) but not in control subjects. The attenuated vascular response to ACh infusion during hypoxia inversely correlated with increased pulmonary artery systolic pressure (p = 0.04) and decreased plasma nitrite correlated with attenuated ACh-induced vasodilation in HAPE-S subjects (p = 0.02).
Hypoxia markedly impairs vascular endothelial function in the systemic circulation in HAPE-S subjects due to a decreased bioavailability of NO. Impairment of the NO pathway could contribute to the enhanced hypoxic pulmonary vasoconstriction that is central to the pathogenesis of HAPE. |
| doi_str_mv | 10.1164/rccm.200504-654OC |
| format | Article |
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We hypothesized that individuals susceptible to HAPE (HAPE-S) would also have dysfunction of the vascular NO vasodilator pathway during hypoxia in the systemic vasculature.
During normoxia (FI(O(2)) = 0.21) and 4 hours of normobaric hypoxia (FI(O(2)) = 0.12, corresponding to an altitude of 4,500 m above sea level) endothelium-dependent and endothelium-independent vasodilator responses to intraarterial infusion of acetylcholine (ACh) and sodium nitroprusside, respectively, were measured by forearm venous occlusion plethysmography in nine HAPE-S subjects and in nine HAPE-resistant control subjects.
Pulmonary artery systolic pressure increased from 22 +/- 3 to 33 +/- 6 mm Hg (p < 0.001) during hypoxia in control subjects, and from 25 +/- 4 to 50 +/- 9 mm Hg in HAPE-S subjects (p < 0.001). Despite similar responses during normoxia in both groups, ACh-induced changes in forearm blood flow markedly decreased during hypoxia in HAPE-S subjects (p = 0.01) but not in control subjects. The attenuated vascular response to ACh infusion during hypoxia inversely correlated with increased pulmonary artery systolic pressure (p = 0.04) and decreased plasma nitrite correlated with attenuated ACh-induced vasodilation in HAPE-S subjects (p = 0.02).
Hypoxia markedly impairs vascular endothelial function in the systemic circulation in HAPE-S subjects due to a decreased bioavailability of NO. Impairment of the NO pathway could contribute to the enhanced hypoxic pulmonary vasoconstriction that is central to the pathogenesis of HAPE.</description><identifier>ISSN: 1073-449X</identifier><identifier>EISSN: 1535-4970</identifier><identifier>DOI: 10.1164/rccm.200504-654OC</identifier><identifier>PMID: 15947284</identifier><language>eng</language><publisher>New York, NY: Am Thoracic Soc</publisher><subject>Acetylcholine - pharmacology ; Adult ; Altitude Sickness - etiology ; Anesthesia. Intensive care medicine. Transfusions. Cell therapy and gene therapy ; Arterial hypertension. Arterial hypotension ; Biological and medical sciences ; Blood and lymphatic vessels ; Blood Pressure ; Cardiology. Vascular system ; Clinical manifestations. Epidemiology. Investigative techniques. Etiology ; Disease Susceptibility ; Endothelin-1 - blood ; Endothelium, Vascular - physiopathology ; Female ; Forearm - blood supply ; Hemodynamics ; Humans ; Hypoxia - blood ; Hypoxia - physiopathology ; Intensive care medicine ; Male ; Medical sciences ; Middle Aged ; Nitrates - blood ; Nitrites - blood ; Nitroprusside - pharmacology ; Pneumology ; Pulmonary Artery - physiopathology ; Pulmonary Edema - etiology ; Pulmonary Gas Exchange ; Pulmonary hypertension. Acute cor pulmonale. Pulmonary embolism. Pulmonary vascular diseases ; Regional Blood Flow ; Single-Blind Method ; Vasodilation ; Vasodilator Agents - pharmacology</subject><ispartof>American journal of respiratory and critical care medicine, 2005-09, Vol.172 (6), p.763-767</ispartof><rights>2005 INIST-CNRS</rights><rights>Copyright American Thoracic Society Sep 15, 2005</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c390t-53670b9ad642de57cc3c7dd0099950d6bb74ef59c66b410b360348cbd22f2a4c3</citedby><cites>FETCH-LOGICAL-c390t-53670b9ad642de57cc3c7dd0099950d6bb74ef59c66b410b360348cbd22f2a4c3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,4011,4012,27901,27902</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=17108358$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/15947284$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Berger, Marc M</creatorcontrib><creatorcontrib>Hesse, Christiane</creatorcontrib><creatorcontrib>Dehnert, Christoph</creatorcontrib><creatorcontrib>Siedler, Heike</creatorcontrib><creatorcontrib>Kleinbongard, Petra</creatorcontrib><creatorcontrib>Bardenheuer, Hubert J</creatorcontrib><creatorcontrib>Kelm, Malte</creatorcontrib><creatorcontrib>Bartsch, Peter</creatorcontrib><creatorcontrib>Haefeli, Walter E</creatorcontrib><title>Hypoxia Impairs Systemic Endothelial Function in Individuals Prone to High-Altitude Pulmonary Edema</title><title>American journal of respiratory and critical care medicine</title><addtitle>Am J Respir Crit Care Med</addtitle><description>High-altitude pulmonary edema (HAPE) is characterized by excessive pulmonary vasoconstriction and is associated with decreased concentrations of nitric oxide (NO) in the lung.
We hypothesized that individuals susceptible to HAPE (HAPE-S) would also have dysfunction of the vascular NO vasodilator pathway during hypoxia in the systemic vasculature.
During normoxia (FI(O(2)) = 0.21) and 4 hours of normobaric hypoxia (FI(O(2)) = 0.12, corresponding to an altitude of 4,500 m above sea level) endothelium-dependent and endothelium-independent vasodilator responses to intraarterial infusion of acetylcholine (ACh) and sodium nitroprusside, respectively, were measured by forearm venous occlusion plethysmography in nine HAPE-S subjects and in nine HAPE-resistant control subjects.
Pulmonary artery systolic pressure increased from 22 +/- 3 to 33 +/- 6 mm Hg (p < 0.001) during hypoxia in control subjects, and from 25 +/- 4 to 50 +/- 9 mm Hg in HAPE-S subjects (p < 0.001). Despite similar responses during normoxia in both groups, ACh-induced changes in forearm blood flow markedly decreased during hypoxia in HAPE-S subjects (p = 0.01) but not in control subjects. The attenuated vascular response to ACh infusion during hypoxia inversely correlated with increased pulmonary artery systolic pressure (p = 0.04) and decreased plasma nitrite correlated with attenuated ACh-induced vasodilation in HAPE-S subjects (p = 0.02).
Hypoxia markedly impairs vascular endothelial function in the systemic circulation in HAPE-S subjects due to a decreased bioavailability of NO. Impairment of the NO pathway could contribute to the enhanced hypoxic pulmonary vasoconstriction that is central to the pathogenesis of HAPE.</description><subject>Acetylcholine - pharmacology</subject><subject>Adult</subject><subject>Altitude Sickness - etiology</subject><subject>Anesthesia. Intensive care medicine. Transfusions. Cell therapy and gene therapy</subject><subject>Arterial hypertension. Arterial hypotension</subject><subject>Biological and medical sciences</subject><subject>Blood and lymphatic vessels</subject><subject>Blood Pressure</subject><subject>Cardiology. Vascular system</subject><subject>Clinical manifestations. Epidemiology. Investigative techniques. Etiology</subject><subject>Disease Susceptibility</subject><subject>Endothelin-1 - blood</subject><subject>Endothelium, Vascular - physiopathology</subject><subject>Female</subject><subject>Forearm - blood supply</subject><subject>Hemodynamics</subject><subject>Humans</subject><subject>Hypoxia - blood</subject><subject>Hypoxia - physiopathology</subject><subject>Intensive care medicine</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Middle Aged</subject><subject>Nitrates - blood</subject><subject>Nitrites - blood</subject><subject>Nitroprusside - pharmacology</subject><subject>Pneumology</subject><subject>Pulmonary Artery - physiopathology</subject><subject>Pulmonary Edema - etiology</subject><subject>Pulmonary Gas Exchange</subject><subject>Pulmonary hypertension. Acute cor pulmonale. Pulmonary embolism. Pulmonary vascular diseases</subject><subject>Regional Blood Flow</subject><subject>Single-Blind Method</subject><subject>Vasodilation</subject><subject>Vasodilator Agents - pharmacology</subject><issn>1073-449X</issn><issn>1535-4970</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2005</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><recordid>eNpdkE1rGzEQhpfS0KRpf0AvRRRa6GETfWt1DMapDYEEkkJvQitpaxmt5Eq7af3vK9eGQE8zh2femXma5gOCVwhxep2NGa8whAzSljN6v3jVXCBGWEulgK9rDwVpKZU_zpu3pWwhRLhD8E1zjpikAnf0ojGr_S798Rqsx532uYDHfZnc6A1YRpumjQteB3A7RzP5FIGPYB2tf_Z21qGAh5yiA1MCK_9z096EyU-zdeBhDmOKOu_B0rpRv2vOhkq796d62Xy_XT4tVu3d_bf14uauNUTCqWWEC9hLbTnF1jFhDDHCWgillAxa3veCuoFJw3lPEewJh4R2prcYD1hTQy6bL8fcXU6_ZlcmNfpiXAg6ujQXxTvGJOOigp_-A7dpzrHeppCUnGOKuwqhI2RyKiW7Qe2yH-tTCkF10K8O-tVRv_qnv858PAXP_ejsy8TJdwU-nwBdjA5D1tH48sIJBDvCDsu_HrlNFfvbZ6fKqEOosUjp7WExElhxJTghfwHax5zV</recordid><startdate>20050915</startdate><enddate>20050915</enddate><creator>Berger, Marc M</creator><creator>Hesse, Christiane</creator><creator>Dehnert, Christoph</creator><creator>Siedler, Heike</creator><creator>Kleinbongard, Petra</creator><creator>Bardenheuer, Hubert J</creator><creator>Kelm, Malte</creator><creator>Bartsch, Peter</creator><creator>Haefeli, Walter E</creator><general>Am Thoracic Soc</general><general>American Lung Association</general><general>American Thoracic Society</general><scope>IQODW</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>7RV</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8C1</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AN0</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>K9.</scope><scope>KB0</scope><scope>M0S</scope><scope>M1P</scope><scope>NAPCQ</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope></search><sort><creationdate>20050915</creationdate><title>Hypoxia Impairs Systemic Endothelial Function in Individuals Prone to High-Altitude Pulmonary Edema</title><author>Berger, Marc M ; Hesse, Christiane ; Dehnert, Christoph ; Siedler, Heike ; Kleinbongard, Petra ; Bardenheuer, Hubert J ; Kelm, Malte ; Bartsch, Peter ; Haefeli, Walter E</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c390t-53670b9ad642de57cc3c7dd0099950d6bb74ef59c66b410b360348cbd22f2a4c3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2005</creationdate><topic>Acetylcholine - pharmacology</topic><topic>Adult</topic><topic>Altitude Sickness - etiology</topic><topic>Anesthesia. Intensive care medicine. Transfusions. Cell therapy and gene therapy</topic><topic>Arterial hypertension. Arterial hypotension</topic><topic>Biological and medical sciences</topic><topic>Blood and lymphatic vessels</topic><topic>Blood Pressure</topic><topic>Cardiology. Vascular system</topic><topic>Clinical manifestations. Epidemiology. Investigative techniques. Etiology</topic><topic>Disease Susceptibility</topic><topic>Endothelin-1 - blood</topic><topic>Endothelium, Vascular - physiopathology</topic><topic>Female</topic><topic>Forearm - blood supply</topic><topic>Hemodynamics</topic><topic>Humans</topic><topic>Hypoxia - blood</topic><topic>Hypoxia - physiopathology</topic><topic>Intensive care medicine</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Middle Aged</topic><topic>Nitrates - blood</topic><topic>Nitrites - blood</topic><topic>Nitroprusside - pharmacology</topic><topic>Pneumology</topic><topic>Pulmonary Artery - physiopathology</topic><topic>Pulmonary Edema - etiology</topic><topic>Pulmonary Gas Exchange</topic><topic>Pulmonary hypertension. Acute cor pulmonale. Pulmonary embolism. 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We hypothesized that individuals susceptible to HAPE (HAPE-S) would also have dysfunction of the vascular NO vasodilator pathway during hypoxia in the systemic vasculature.
During normoxia (FI(O(2)) = 0.21) and 4 hours of normobaric hypoxia (FI(O(2)) = 0.12, corresponding to an altitude of 4,500 m above sea level) endothelium-dependent and endothelium-independent vasodilator responses to intraarterial infusion of acetylcholine (ACh) and sodium nitroprusside, respectively, were measured by forearm venous occlusion plethysmography in nine HAPE-S subjects and in nine HAPE-resistant control subjects.
Pulmonary artery systolic pressure increased from 22 +/- 3 to 33 +/- 6 mm Hg (p < 0.001) during hypoxia in control subjects, and from 25 +/- 4 to 50 +/- 9 mm Hg in HAPE-S subjects (p < 0.001). Despite similar responses during normoxia in both groups, ACh-induced changes in forearm blood flow markedly decreased during hypoxia in HAPE-S subjects (p = 0.01) but not in control subjects. The attenuated vascular response to ACh infusion during hypoxia inversely correlated with increased pulmonary artery systolic pressure (p = 0.04) and decreased plasma nitrite correlated with attenuated ACh-induced vasodilation in HAPE-S subjects (p = 0.02).
Hypoxia markedly impairs vascular endothelial function in the systemic circulation in HAPE-S subjects due to a decreased bioavailability of NO. Impairment of the NO pathway could contribute to the enhanced hypoxic pulmonary vasoconstriction that is central to the pathogenesis of HAPE.</abstract><cop>New York, NY</cop><pub>Am Thoracic Soc</pub><pmid>15947284</pmid><doi>10.1164/rccm.200504-654OC</doi><tpages>5</tpages></addata></record> |
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| ispartof | American journal of respiratory and critical care medicine, 2005-09, Vol.172 (6), p.763-767 |
| issn | 1073-449X 1535-4970 |
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| source | Journals@Ovid Ovid Autoload; MEDLINE; American Thoracic Society (ATS) Journals Online; EZB-FREE-00999 freely available EZB journals; Alma/SFX Local Collection |
| subjects | Acetylcholine - pharmacology Adult Altitude Sickness - etiology Anesthesia. Intensive care medicine. Transfusions. Cell therapy and gene therapy Arterial hypertension. Arterial hypotension Biological and medical sciences Blood and lymphatic vessels Blood Pressure Cardiology. Vascular system Clinical manifestations. Epidemiology. Investigative techniques. Etiology Disease Susceptibility Endothelin-1 - blood Endothelium, Vascular - physiopathology Female Forearm - blood supply Hemodynamics Humans Hypoxia - blood Hypoxia - physiopathology Intensive care medicine Male Medical sciences Middle Aged Nitrates - blood Nitrites - blood Nitroprusside - pharmacology Pneumology Pulmonary Artery - physiopathology Pulmonary Edema - etiology Pulmonary Gas Exchange Pulmonary hypertension. Acute cor pulmonale. Pulmonary embolism. Pulmonary vascular diseases Regional Blood Flow Single-Blind Method Vasodilation Vasodilator Agents - pharmacology |
| title | Hypoxia Impairs Systemic Endothelial Function in Individuals Prone to High-Altitude Pulmonary Edema |
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