Selective potentiation of peripheral chemoreflex sensitivity in obstructive sleep apnea
The chemoreflexes are an important mechanism for regulation of both breathing and autonomic cardiovascular function. Abnormalities in chemoreflex mechanisms may be implicated in increased cardiovascular stress in patients with obstructive sleep apnea (OSA). We tested the hypothesis that chemoreflex...
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Veröffentlicht in: | Circulation (New York, N.Y.) N.Y.), 1999-03, Vol.99 (9), p.1183-1189 |
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creator | NARKIEWICZ, K VAN DE BORNE, P. J. H PESEK, C. A DYKEN, M. E MONTANO, N SOMERS, V. K |
description | The chemoreflexes are an important mechanism for regulation of both breathing and autonomic cardiovascular function. Abnormalities in chemoreflex mechanisms may be implicated in increased cardiovascular stress in patients with obstructive sleep apnea (OSA). We tested the hypothesis that chemoreflex function is altered in patients with OSA.
We compared ventilatory, sympathetic, heart rate, and blood pressure responses to hypoxia, hypercapnia, and the cold pressor test in 16 untreated normotensive patients with OSA and 12 normal control subjects matched for age and body mass index. Baseline muscle sympathetic nerve activity (MSNA) was higher in the patients with OSA than in the control subjects (43+/-4 versus 21+/-3 bursts per minute; P |
doi_str_mv | 10.1161/01.cir.99.9.1183 |
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We compared ventilatory, sympathetic, heart rate, and blood pressure responses to hypoxia, hypercapnia, and the cold pressor test in 16 untreated normotensive patients with OSA and 12 normal control subjects matched for age and body mass index. Baseline muscle sympathetic nerve activity (MSNA) was higher in the patients with OSA than in the control subjects (43+/-4 versus 21+/-3 bursts per minute; P<0. 001). During hypoxia, patients with OSA had greater increases in minute ventilation (5.8+/-0.8 versus 3.2+/-0.7 L/min; P=0.02), heart rate (10+/-1 versus 7+/-1 bpm; P=0.03), and mean arterial pressure (7+/-2 versus 0+/-2 mm Hg; P=0.001) than control subjects. Despite higher ventilation and blood pressure (both of which inhibit sympathetic activity) in OSA patients, the MSNA increase during hypoxia was similar in OSA patients and control subjects. When the sympathetic-inhibitory influence of breathing was eliminated by apnea during hypoxia, the increase in MSNA in OSA patients (106+/-20%) was greater than in control subjects (52+/-23%; P=0.04). Prolongation of R-R interval with apnea during hypoxia was also greater in OSA patients (24+/-6%) than in control subjects (7+/-5%) (P=0.04). Autonomic, ventilatory, and blood pressure responses to hypercapnia and the cold pressor test in OSA patients were not different from those observed in control subjects.
OSA is associated with a selective potentiation of autonomic, hemodynamic, and ventilatory responses to peripheral chemoreceptor activation by hypoxia.</description><identifier>ISSN: 0009-7322</identifier><identifier>EISSN: 1524-4539</identifier><identifier>DOI: 10.1161/01.cir.99.9.1183</identifier><identifier>PMID: 10069786</identifier><identifier>CODEN: CIRCAZ</identifier><language>eng</language><publisher>Hagerstown, MD: Lippincott Williams & Wilkins</publisher><subject>Adult ; Autonomic Nervous System - physiopathology ; Biological and medical sciences ; Blood Pressure - physiology ; Chemoreceptor Cells - physiology ; Cold Temperature ; Female ; Humans ; Hypercapnia - physiopathology ; Hypoxia - physiopathology ; Male ; Medical sciences ; Pneumology ; Reflex - physiology ; Respiratory Mechanics - physiology ; Respiratory system : syndromes and miscellaneous diseases ; Rest - physiology ; Sleep Apnea Syndromes - physiopathology</subject><ispartof>Circulation (New York, N.Y.), 1999-03, Vol.99 (9), p.1183-1189</ispartof><rights>1999 INIST-CNRS</rights><rights>Copyright American Heart Association, Inc. Mar 9, 1999</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c547t-a050e64670f86cefbbe5ed1cdaad9c103a4a6aa407092ae3423c7ba45a985dea3</citedby><cites>FETCH-LOGICAL-c547t-a050e64670f86cefbbe5ed1cdaad9c103a4a6aa407092ae3423c7ba45a985dea3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,3674,27901,27902</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=1708712$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/10069786$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>NARKIEWICZ, K</creatorcontrib><creatorcontrib>VAN DE BORNE, P. J. H</creatorcontrib><creatorcontrib>PESEK, C. A</creatorcontrib><creatorcontrib>DYKEN, M. E</creatorcontrib><creatorcontrib>MONTANO, N</creatorcontrib><creatorcontrib>SOMERS, V. K</creatorcontrib><title>Selective potentiation of peripheral chemoreflex sensitivity in obstructive sleep apnea</title><title>Circulation (New York, N.Y.)</title><addtitle>Circulation</addtitle><description>The chemoreflexes are an important mechanism for regulation of both breathing and autonomic cardiovascular function. Abnormalities in chemoreflex mechanisms may be implicated in increased cardiovascular stress in patients with obstructive sleep apnea (OSA). We tested the hypothesis that chemoreflex function is altered in patients with OSA.
We compared ventilatory, sympathetic, heart rate, and blood pressure responses to hypoxia, hypercapnia, and the cold pressor test in 16 untreated normotensive patients with OSA and 12 normal control subjects matched for age and body mass index. Baseline muscle sympathetic nerve activity (MSNA) was higher in the patients with OSA than in the control subjects (43+/-4 versus 21+/-3 bursts per minute; P<0. 001). During hypoxia, patients with OSA had greater increases in minute ventilation (5.8+/-0.8 versus 3.2+/-0.7 L/min; P=0.02), heart rate (10+/-1 versus 7+/-1 bpm; P=0.03), and mean arterial pressure (7+/-2 versus 0+/-2 mm Hg; P=0.001) than control subjects. Despite higher ventilation and blood pressure (both of which inhibit sympathetic activity) in OSA patients, the MSNA increase during hypoxia was similar in OSA patients and control subjects. When the sympathetic-inhibitory influence of breathing was eliminated by apnea during hypoxia, the increase in MSNA in OSA patients (106+/-20%) was greater than in control subjects (52+/-23%; P=0.04). Prolongation of R-R interval with apnea during hypoxia was also greater in OSA patients (24+/-6%) than in control subjects (7+/-5%) (P=0.04). Autonomic, ventilatory, and blood pressure responses to hypercapnia and the cold pressor test in OSA patients were not different from those observed in control subjects.
OSA is associated with a selective potentiation of autonomic, hemodynamic, and ventilatory responses to peripheral chemoreceptor activation by hypoxia.</description><subject>Adult</subject><subject>Autonomic Nervous System - physiopathology</subject><subject>Biological and medical sciences</subject><subject>Blood Pressure - physiology</subject><subject>Chemoreceptor Cells - physiology</subject><subject>Cold Temperature</subject><subject>Female</subject><subject>Humans</subject><subject>Hypercapnia - physiopathology</subject><subject>Hypoxia - physiopathology</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Pneumology</subject><subject>Reflex - physiology</subject><subject>Respiratory Mechanics - physiology</subject><subject>Respiratory system : syndromes and miscellaneous diseases</subject><subject>Rest - physiology</subject><subject>Sleep Apnea Syndromes - physiopathology</subject><issn>0009-7322</issn><issn>1524-4539</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1999</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpdkEtLxDAUhYMoOj72rqSIuOuYR5M0Sxl8gSD4wGW4TW8x0mlr0orz743MgOLqPvjO4d5DyDGjc8YUu6Bs7nyYGzM3aVGKLTJjkhd5IYXZJjNKqcm14HyP7Mf4nkYltNwleyx1RpdqRl6fsEU3-k_Mhn7EbvQw-r7L-iYbMPjhDQO0mXvDZR-wafEri9hFnwR-XGU-gVUcw7R2iC3ikMHQIRySnQbaiEebekBerq-eF7f5_cPN3eLyPney0GMOVFJUhdK0KZXDpqpQYs1cDVAbx6iAAhRAQTU1HFAUXDhdQSHBlLJGEAfkfO07hP5jwjjapY8O2xY67KdolVFMKMETePoPfO-n0KXbLGdclVQykSC6hlzoY0wP2yH4JYSVZdT-JG4ps4u7R2uMNfYn8SQ52fhO1RLrP4J1xAk42wAQHbRNgM75-MtpWmrGxTfbvor9</recordid><startdate>19990309</startdate><enddate>19990309</enddate><creator>NARKIEWICZ, K</creator><creator>VAN DE BORNE, P. J. H</creator><creator>PESEK, C. A</creator><creator>DYKEN, M. E</creator><creator>MONTANO, N</creator><creator>SOMERS, V. K</creator><general>Lippincott Williams & Wilkins</general><general>American Heart Association, Inc</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>K9.</scope><scope>NAPCQ</scope><scope>U9A</scope><scope>7X8</scope></search><sort><creationdate>19990309</creationdate><title>Selective potentiation of peripheral chemoreflex sensitivity in obstructive sleep apnea</title><author>NARKIEWICZ, K ; VAN DE BORNE, P. J. H ; PESEK, C. A ; DYKEN, M. E ; MONTANO, N ; SOMERS, V. K</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c547t-a050e64670f86cefbbe5ed1cdaad9c103a4a6aa407092ae3423c7ba45a985dea3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1999</creationdate><topic>Adult</topic><topic>Autonomic Nervous System - physiopathology</topic><topic>Biological and medical sciences</topic><topic>Blood Pressure - physiology</topic><topic>Chemoreceptor Cells - physiology</topic><topic>Cold Temperature</topic><topic>Female</topic><topic>Humans</topic><topic>Hypercapnia - physiopathology</topic><topic>Hypoxia - physiopathology</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Pneumology</topic><topic>Reflex - physiology</topic><topic>Respiratory Mechanics - physiology</topic><topic>Respiratory system : syndromes and miscellaneous diseases</topic><topic>Rest - physiology</topic><topic>Sleep Apnea Syndromes - physiopathology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>NARKIEWICZ, K</creatorcontrib><creatorcontrib>VAN DE BORNE, P. J. H</creatorcontrib><creatorcontrib>PESEK, C. A</creatorcontrib><creatorcontrib>DYKEN, M. E</creatorcontrib><creatorcontrib>MONTANO, N</creatorcontrib><creatorcontrib>SOMERS, V. K</creatorcontrib><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Nursing & Allied Health Premium</collection><collection>MEDLINE - Academic</collection><jtitle>Circulation (New York, N.Y.)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>NARKIEWICZ, K</au><au>VAN DE BORNE, P. J. H</au><au>PESEK, C. A</au><au>DYKEN, M. E</au><au>MONTANO, N</au><au>SOMERS, V. K</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Selective potentiation of peripheral chemoreflex sensitivity in obstructive sleep apnea</atitle><jtitle>Circulation (New York, N.Y.)</jtitle><addtitle>Circulation</addtitle><date>1999-03-09</date><risdate>1999</risdate><volume>99</volume><issue>9</issue><spage>1183</spage><epage>1189</epage><pages>1183-1189</pages><issn>0009-7322</issn><eissn>1524-4539</eissn><coden>CIRCAZ</coden><abstract>The chemoreflexes are an important mechanism for regulation of both breathing and autonomic cardiovascular function. Abnormalities in chemoreflex mechanisms may be implicated in increased cardiovascular stress in patients with obstructive sleep apnea (OSA). We tested the hypothesis that chemoreflex function is altered in patients with OSA.
We compared ventilatory, sympathetic, heart rate, and blood pressure responses to hypoxia, hypercapnia, and the cold pressor test in 16 untreated normotensive patients with OSA and 12 normal control subjects matched for age and body mass index. Baseline muscle sympathetic nerve activity (MSNA) was higher in the patients with OSA than in the control subjects (43+/-4 versus 21+/-3 bursts per minute; P<0. 001). During hypoxia, patients with OSA had greater increases in minute ventilation (5.8+/-0.8 versus 3.2+/-0.7 L/min; P=0.02), heart rate (10+/-1 versus 7+/-1 bpm; P=0.03), and mean arterial pressure (7+/-2 versus 0+/-2 mm Hg; P=0.001) than control subjects. Despite higher ventilation and blood pressure (both of which inhibit sympathetic activity) in OSA patients, the MSNA increase during hypoxia was similar in OSA patients and control subjects. When the sympathetic-inhibitory influence of breathing was eliminated by apnea during hypoxia, the increase in MSNA in OSA patients (106+/-20%) was greater than in control subjects (52+/-23%; P=0.04). Prolongation of R-R interval with apnea during hypoxia was also greater in OSA patients (24+/-6%) than in control subjects (7+/-5%) (P=0.04). Autonomic, ventilatory, and blood pressure responses to hypercapnia and the cold pressor test in OSA patients were not different from those observed in control subjects.
OSA is associated with a selective potentiation of autonomic, hemodynamic, and ventilatory responses to peripheral chemoreceptor activation by hypoxia.</abstract><cop>Hagerstown, MD</cop><pub>Lippincott Williams & Wilkins</pub><pmid>10069786</pmid><doi>10.1161/01.cir.99.9.1183</doi><tpages>7</tpages><oa>free_for_read</oa></addata></record> |
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subjects | Adult Autonomic Nervous System - physiopathology Biological and medical sciences Blood Pressure - physiology Chemoreceptor Cells - physiology Cold Temperature Female Humans Hypercapnia - physiopathology Hypoxia - physiopathology Male Medical sciences Pneumology Reflex - physiology Respiratory Mechanics - physiology Respiratory system : syndromes and miscellaneous diseases Rest - physiology Sleep Apnea Syndromes - physiopathology |
title | Selective potentiation of peripheral chemoreflex sensitivity in obstructive sleep apnea |
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