Reduced baroreflex sensitivity and pulmonary dysfunction in alcoholic cirrhosis: effect of hyperoxia
Patients with cirrhosis exhibit impaired regulation of the arterial blood pressure, reduced baroreflex sensitivity (BRS), and prolonged QT interval. In addition, a considerable number of patients have a pulmonary dysfunction with hypoxemia, impaired lung diffusing capacity (Dl(CO)), and presence of...
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Veröffentlicht in: | American journal of physiology: Gastrointestinal and liver physiology 2010-09, Vol.299 (3), p.G784-G790 |
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creator | Møller, Søren Iversen, Jens S Krag, Aleksander Bie, Peter Kjaer, Andreas Bendtsen, Flemming |
description | Patients with cirrhosis exhibit impaired regulation of the arterial blood pressure, reduced baroreflex sensitivity (BRS), and prolonged QT interval. In addition, a considerable number of patients have a pulmonary dysfunction with hypoxemia, impaired lung diffusing capacity (Dl(CO)), and presence of hepatopulmonary syndrome (HPS). BRS is reduced at exposure to chronic hypoxia such as during sojourn in high altitudes. In this study, we assessed the relation of BRS to pulmonary dysfunction and cardiovascular characteristics and the effects of hyperoxia. Forty-three patients with cirrhosis and 12 healthy matched controls underwent hemodynamic and pulmonary investigations. BRS was assessed by cross-spectral analysis of variabilities between blood pressure and heart rate time series. A 100% oxygen test was performed with the assessment of arterial oxygen tensions (Pa(O(2))) and alveolar-arterial oxygen gradient. Baseline BRS was significantly reduced in the cirrhotic patients compared with the controls (4.7 +/- 0.8 vs. 10.3 +/- 2.0 ms/mmHg; P < 0.001). The frequency-corrected QT interval was significantly prolonged in the cirrhotic patients (P < 0.05). There was no significant difference in BRS according to presence of HPS, Pa(O(2)), Dl(CO), or Child-Turcotte score, but BRS correlated with metabolic and hemodynamic characteristics. After 100% oxygen inhalation, BRS and the QT interval remained unchanged in the cirrhotic patients. In conclusion, BRS is significantly reduced in patients with cirrhosis compared with controls, but it is unrelated to the degree of pulmonary dysfunction and portal hypertension. Acute hyperoxia does not significantly revert the low BRS or the prolonged QT interval in cirrhosis. |
doi_str_mv | 10.1152/ajpgi.00078.2010 |
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In addition, a considerable number of patients have a pulmonary dysfunction with hypoxemia, impaired lung diffusing capacity (Dl(CO)), and presence of hepatopulmonary syndrome (HPS). BRS is reduced at exposure to chronic hypoxia such as during sojourn in high altitudes. In this study, we assessed the relation of BRS to pulmonary dysfunction and cardiovascular characteristics and the effects of hyperoxia. Forty-three patients with cirrhosis and 12 healthy matched controls underwent hemodynamic and pulmonary investigations. BRS was assessed by cross-spectral analysis of variabilities between blood pressure and heart rate time series. A 100% oxygen test was performed with the assessment of arterial oxygen tensions (Pa(O(2))) and alveolar-arterial oxygen gradient. Baseline BRS was significantly reduced in the cirrhotic patients compared with the controls (4.7 +/- 0.8 vs. 10.3 +/- 2.0 ms/mmHg; P < 0.001). The frequency-corrected QT interval was significantly prolonged in the cirrhotic patients (P < 0.05). There was no significant difference in BRS according to presence of HPS, Pa(O(2)), Dl(CO), or Child-Turcotte score, but BRS correlated with metabolic and hemodynamic characteristics. After 100% oxygen inhalation, BRS and the QT interval remained unchanged in the cirrhotic patients. In conclusion, BRS is significantly reduced in patients with cirrhosis compared with controls, but it is unrelated to the degree of pulmonary dysfunction and portal hypertension. Acute hyperoxia does not significantly revert the low BRS or the prolonged QT interval in cirrhosis.</description><identifier>ISSN: 0193-1857</identifier><identifier>EISSN: 1522-1547</identifier><identifier>DOI: 10.1152/ajpgi.00078.2010</identifier><identifier>PMID: 20616307</identifier><identifier>CODEN: APGPDF</identifier><language>eng</language><publisher>United States: American Physiological Society</publisher><subject>Aged ; Aldosterone - blood ; Angiotensin II - metabolism ; Atrial Natriuretic Factor - blood ; Baroreflex - physiology ; Blood pressure ; Case-Control Studies ; Endothelin-1 - blood ; Female ; Humans ; Hyperoxia ; Liver cirrhosis ; Liver Cirrhosis, Alcoholic - complications ; Lung Diseases - etiology ; Lung Diseases - therapy ; Male ; Middle Aged ; Natriuretic Peptide, Brain - blood ; Norepinephrine - blood ; Oxygen ; Oxygen - therapeutic use ; Physiology ; Pulmonary arteries ; Renin - blood</subject><ispartof>American journal of physiology: Gastrointestinal and liver physiology, 2010-09, Vol.299 (3), p.G784-G790</ispartof><rights>Copyright American Physiological Society Sep 2010</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c325t-473feb8ea9a1e02151f6424621ed7227d833292d12266f245d274f924055ad3d3</citedby><cites>FETCH-LOGICAL-c325t-473feb8ea9a1e02151f6424621ed7227d833292d12266f245d274f924055ad3d3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,3037,27923,27924</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/20616307$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Møller, Søren</creatorcontrib><creatorcontrib>Iversen, Jens S</creatorcontrib><creatorcontrib>Krag, Aleksander</creatorcontrib><creatorcontrib>Bie, Peter</creatorcontrib><creatorcontrib>Kjaer, Andreas</creatorcontrib><creatorcontrib>Bendtsen, Flemming</creatorcontrib><title>Reduced baroreflex sensitivity and pulmonary dysfunction in alcoholic cirrhosis: effect of hyperoxia</title><title>American journal of physiology: Gastrointestinal and liver physiology</title><addtitle>Am J Physiol Gastrointest Liver Physiol</addtitle><description>Patients with cirrhosis exhibit impaired regulation of the arterial blood pressure, reduced baroreflex sensitivity (BRS), and prolonged QT interval. In addition, a considerable number of patients have a pulmonary dysfunction with hypoxemia, impaired lung diffusing capacity (Dl(CO)), and presence of hepatopulmonary syndrome (HPS). BRS is reduced at exposure to chronic hypoxia such as during sojourn in high altitudes. In this study, we assessed the relation of BRS to pulmonary dysfunction and cardiovascular characteristics and the effects of hyperoxia. Forty-three patients with cirrhosis and 12 healthy matched controls underwent hemodynamic and pulmonary investigations. BRS was assessed by cross-spectral analysis of variabilities between blood pressure and heart rate time series. A 100% oxygen test was performed with the assessment of arterial oxygen tensions (Pa(O(2))) and alveolar-arterial oxygen gradient. Baseline BRS was significantly reduced in the cirrhotic patients compared with the controls (4.7 +/- 0.8 vs. 10.3 +/- 2.0 ms/mmHg; P < 0.001). The frequency-corrected QT interval was significantly prolonged in the cirrhotic patients (P < 0.05). There was no significant difference in BRS according to presence of HPS, Pa(O(2)), Dl(CO), or Child-Turcotte score, but BRS correlated with metabolic and hemodynamic characteristics. After 100% oxygen inhalation, BRS and the QT interval remained unchanged in the cirrhotic patients. In conclusion, BRS is significantly reduced in patients with cirrhosis compared with controls, but it is unrelated to the degree of pulmonary dysfunction and portal hypertension. Acute hyperoxia does not significantly revert the low BRS or the prolonged QT interval in cirrhosis.</description><subject>Aged</subject><subject>Aldosterone - blood</subject><subject>Angiotensin II - metabolism</subject><subject>Atrial Natriuretic Factor - blood</subject><subject>Baroreflex - physiology</subject><subject>Blood pressure</subject><subject>Case-Control Studies</subject><subject>Endothelin-1 - blood</subject><subject>Female</subject><subject>Humans</subject><subject>Hyperoxia</subject><subject>Liver cirrhosis</subject><subject>Liver Cirrhosis, Alcoholic - complications</subject><subject>Lung Diseases - etiology</subject><subject>Lung Diseases - therapy</subject><subject>Male</subject><subject>Middle Aged</subject><subject>Natriuretic Peptide, Brain - blood</subject><subject>Norepinephrine - blood</subject><subject>Oxygen</subject><subject>Oxygen - therapeutic use</subject><subject>Physiology</subject><subject>Pulmonary arteries</subject><subject>Renin - blood</subject><issn>0193-1857</issn><issn>1522-1547</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2010</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpdkEuLFDEUhYM4OO3o3pUEN7OqntybV7c7GRwVBgTRdZFObuw01ZUyqZLpf2_moQtXFw7fOVw-xt6AWANovHKH6WdaCyHsZo0CxDO2ajF2oJV9zlYCtrKDjbbn7GWth8ZpBHjBzlEYMFLYFQvfKCyeAt-5kgvFge54pbGmOf1O84m7MfBpGY55dOXEw6nGZfRzyiNPI3eDz_s8JM99KmWfa6rvOcVIfuY58v1popLvknvFzqIbKr1-uhfsx83H79efu9uvn75cf7jtvEQ9d8rKSLsNua0DEggaolGoDAIFi2jDRkrcYgBEYyIqHdCquEUltHZBBnnBLh93p5J_LVTn_piqp2FwI-Wl9lYrAaDQNPLdf-QhL2VszzVISG2NEQ0Sj5AvudYmp59KOjYPPYj-3n__4L9_8N_f-2-Vt0-7y-5I4V_hr3D5B2Uigcc</recordid><startdate>201009</startdate><enddate>201009</enddate><creator>Møller, Søren</creator><creator>Iversen, Jens S</creator><creator>Krag, Aleksander</creator><creator>Bie, Peter</creator><creator>Kjaer, Andreas</creator><creator>Bendtsen, Flemming</creator><general>American Physiological Society</general><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>7X8</scope></search><sort><creationdate>201009</creationdate><title>Reduced baroreflex sensitivity and pulmonary dysfunction in alcoholic cirrhosis: effect of hyperoxia</title><author>Møller, Søren ; Iversen, Jens S ; Krag, Aleksander ; Bie, Peter ; Kjaer, Andreas ; Bendtsen, Flemming</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c325t-473feb8ea9a1e02151f6424621ed7227d833292d12266f245d274f924055ad3d3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2010</creationdate><topic>Aged</topic><topic>Aldosterone - blood</topic><topic>Angiotensin II - metabolism</topic><topic>Atrial Natriuretic Factor - blood</topic><topic>Baroreflex - physiology</topic><topic>Blood pressure</topic><topic>Case-Control Studies</topic><topic>Endothelin-1 - blood</topic><topic>Female</topic><topic>Humans</topic><topic>Hyperoxia</topic><topic>Liver cirrhosis</topic><topic>Liver Cirrhosis, Alcoholic - complications</topic><topic>Lung Diseases - etiology</topic><topic>Lung Diseases - therapy</topic><topic>Male</topic><topic>Middle Aged</topic><topic>Natriuretic Peptide, Brain - blood</topic><topic>Norepinephrine - blood</topic><topic>Oxygen</topic><topic>Oxygen - therapeutic use</topic><topic>Physiology</topic><topic>Pulmonary arteries</topic><topic>Renin - blood</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Møller, Søren</creatorcontrib><creatorcontrib>Iversen, Jens S</creatorcontrib><creatorcontrib>Krag, Aleksander</creatorcontrib><creatorcontrib>Bie, Peter</creatorcontrib><creatorcontrib>Kjaer, Andreas</creatorcontrib><creatorcontrib>Bendtsen, Flemming</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>American journal of physiology: Gastrointestinal and liver physiology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Møller, Søren</au><au>Iversen, Jens S</au><au>Krag, Aleksander</au><au>Bie, Peter</au><au>Kjaer, Andreas</au><au>Bendtsen, Flemming</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Reduced baroreflex sensitivity and pulmonary dysfunction in alcoholic cirrhosis: effect of hyperoxia</atitle><jtitle>American journal of physiology: Gastrointestinal and liver physiology</jtitle><addtitle>Am J Physiol Gastrointest Liver Physiol</addtitle><date>2010-09</date><risdate>2010</risdate><volume>299</volume><issue>3</issue><spage>G784</spage><epage>G790</epage><pages>G784-G790</pages><issn>0193-1857</issn><eissn>1522-1547</eissn><coden>APGPDF</coden><abstract>Patients with cirrhosis exhibit impaired regulation of the arterial blood pressure, reduced baroreflex sensitivity (BRS), and prolonged QT interval. In addition, a considerable number of patients have a pulmonary dysfunction with hypoxemia, impaired lung diffusing capacity (Dl(CO)), and presence of hepatopulmonary syndrome (HPS). BRS is reduced at exposure to chronic hypoxia such as during sojourn in high altitudes. In this study, we assessed the relation of BRS to pulmonary dysfunction and cardiovascular characteristics and the effects of hyperoxia. Forty-three patients with cirrhosis and 12 healthy matched controls underwent hemodynamic and pulmonary investigations. BRS was assessed by cross-spectral analysis of variabilities between blood pressure and heart rate time series. A 100% oxygen test was performed with the assessment of arterial oxygen tensions (Pa(O(2))) and alveolar-arterial oxygen gradient. Baseline BRS was significantly reduced in the cirrhotic patients compared with the controls (4.7 +/- 0.8 vs. 10.3 +/- 2.0 ms/mmHg; P < 0.001). The frequency-corrected QT interval was significantly prolonged in the cirrhotic patients (P < 0.05). There was no significant difference in BRS according to presence of HPS, Pa(O(2)), Dl(CO), or Child-Turcotte score, but BRS correlated with metabolic and hemodynamic characteristics. After 100% oxygen inhalation, BRS and the QT interval remained unchanged in the cirrhotic patients. In conclusion, BRS is significantly reduced in patients with cirrhosis compared with controls, but it is unrelated to the degree of pulmonary dysfunction and portal hypertension. Acute hyperoxia does not significantly revert the low BRS or the prolonged QT interval in cirrhosis.</abstract><cop>United States</cop><pub>American Physiological Society</pub><pmid>20616307</pmid><doi>10.1152/ajpgi.00078.2010</doi></addata></record> |
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subjects | Aged Aldosterone - blood Angiotensin II - metabolism Atrial Natriuretic Factor - blood Baroreflex - physiology Blood pressure Case-Control Studies Endothelin-1 - blood Female Humans Hyperoxia Liver cirrhosis Liver Cirrhosis, Alcoholic - complications Lung Diseases - etiology Lung Diseases - therapy Male Middle Aged Natriuretic Peptide, Brain - blood Norepinephrine - blood Oxygen Oxygen - therapeutic use Physiology Pulmonary arteries Renin - blood |
title | Reduced baroreflex sensitivity and pulmonary dysfunction in alcoholic cirrhosis: effect of hyperoxia |
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