Tonic chemoreflex activation does not contribute to elevated muscle sympathetic nerve activity in heart failure
Sympathetic activation in heart failure may be due to an increase in sympathetic excitatory influences or to a decrease in inhibitory signals to the brain stem. Chemoreflex sensitivity may be increased in patients with heart failure. The present study tested the hypothesis that tonic activation of e...
Gespeichert in:
| Veröffentlicht in: | Circulation (New York, N.Y.) N.Y.), 1996-09, Vol.94 (6), p.1325-1328 |
|---|---|
| Hauptverfasser: | , , , , |
| Format: | Artikel |
| Sprache: | eng |
| Schlagworte: | |
| Online-Zugang: | Volltext |
| Tags: |
Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
|
| container_end_page | 1328 |
|---|---|
| container_issue | 6 |
| container_start_page | 1325 |
| container_title | Circulation (New York, N.Y.) |
| container_volume | 94 |
| creator | VAN DE BORNE, P OREN, R ANDERSON, E. A MARK, A. L SOMERS, V. K |
| description | Sympathetic activation in heart failure may be due to an increase in sympathetic excitatory influences or to a decrease in inhibitory signals to the brain stem. Chemoreflex sensitivity may be increased in patients with heart failure. The present study tested the hypothesis that tonic activation of excitatory chemoreceptor afferents contributes to the elevated sympathetic activity in heart failure.
We recorded sympathetic nerve activity to muscle circulation from the peroneal nerve of 12 chronic heart failure patients while the patients were breathing room air and during deactivation of the chemoreceptors while the patients were breathing a 100% O2 gas mixture. All patients except 2 were in class III of the New York Heart Association functional classification. Left ventricular ejection fraction defined by radionuclide ventriculography was 24 +/- 2% (mean +/- SE). We also obtained measurements of resting sympathetic nerve activity in 9 healthy control subjects to document that sympathetic nerve activity was elevated in heart failure subjects. Resting sympathetic nerve activity was 59 +/- 5 bursts/min in heart failure patients versus 36 +/- 4 bursts/min in control subjects (P < .01). In heart failure patients, oxygen administration increased oxygen saturation from 94 +/- 0.9% to 99 +/- 0.3% (P < .0001). This increase in oxygen saturation did not affect resting muscle sympathetic nerve activity (798 +/- 122 U/min while patients breathed room air and 824 +/- 35 U/min during 100% O2 breathing) or blood pressure.
Increased efferent sympathetic activity to muscle circulation in patients with heart failure is not explained by tonic activation of excitatory chemoreflex afferents. |
| doi_str_mv | 10.1161/01.CIR.94.6.1325 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_miscellaneous_78360616</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>78360616</sourcerecordid><originalsourceid>FETCH-LOGICAL-c323t-e31f966ce18359fafc7c99b89111f75dd23e5884e1882536576d8716792e61623</originalsourceid><addsrcrecordid>eNpdkUlrHDEQhUVIcCZO7rkERAi5dVtLazuGIYvBEDD2WWjU1YxMtzSR1Mbz7y0zgw85FcX76lFVD6HPlPSUSnpFaL-9vu3N0MuecibeoA0VbOgGwc1btCGEmE5xxt6jD6U8tFZyJS7QhdaMGa02KN2lGDz2e1hShmmGJ-x8DY-uhhTxmKDgmCr2KdYcdmsFXBOGGRoAI17W4mfA5bgcXN1DbU4R8iOcPEI94hDxHlyueHJhXjN8RO8mNxf4dK6X6P7Xz7vtn-7m7-_r7Y-bznPGawecTkZKD1RzYSY3eeWN2WlDKZ2UGEfGQWg9NF0zwaVQctSKSmUYSCoZv0TfT76HnP6tUKpdQvEwzy5CWotVmkvSyAZ-_Q98SGuObTfLKFOMNKxB5AT5nEppf7KHHBaXj5YS-xKEJdS2IKwZrLQvQbSRL2ffdbfA-Dpw_nzTv511V7ybp-yiD-UV46xdrgR_BnYKkLw</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>212720606</pqid></control><display><type>article</type><title>Tonic chemoreflex activation does not contribute to elevated muscle sympathetic nerve activity in heart failure</title><source>MEDLINE</source><source>American Heart Association Journals</source><source>Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals</source><source>Journals@Ovid Complete</source><creator>VAN DE BORNE, P ; OREN, R ; ANDERSON, E. A ; MARK, A. L ; SOMERS, V. K</creator><creatorcontrib>VAN DE BORNE, P ; OREN, R ; ANDERSON, E. A ; MARK, A. L ; SOMERS, V. K</creatorcontrib><description>Sympathetic activation in heart failure may be due to an increase in sympathetic excitatory influences or to a decrease in inhibitory signals to the brain stem. Chemoreflex sensitivity may be increased in patients with heart failure. The present study tested the hypothesis that tonic activation of excitatory chemoreceptor afferents contributes to the elevated sympathetic activity in heart failure.
We recorded sympathetic nerve activity to muscle circulation from the peroneal nerve of 12 chronic heart failure patients while the patients were breathing room air and during deactivation of the chemoreceptors while the patients were breathing a 100% O2 gas mixture. All patients except 2 were in class III of the New York Heart Association functional classification. Left ventricular ejection fraction defined by radionuclide ventriculography was 24 +/- 2% (mean +/- SE). We also obtained measurements of resting sympathetic nerve activity in 9 healthy control subjects to document that sympathetic nerve activity was elevated in heart failure subjects. Resting sympathetic nerve activity was 59 +/- 5 bursts/min in heart failure patients versus 36 +/- 4 bursts/min in control subjects (P < .01). In heart failure patients, oxygen administration increased oxygen saturation from 94 +/- 0.9% to 99 +/- 0.3% (P < .0001). This increase in oxygen saturation did not affect resting muscle sympathetic nerve activity (798 +/- 122 U/min while patients breathed room air and 824 +/- 35 U/min during 100% O2 breathing) or blood pressure.
Increased efferent sympathetic activity to muscle circulation in patients with heart failure is not explained by tonic activation of excitatory chemoreflex afferents.</description><identifier>ISSN: 0009-7322</identifier><identifier>EISSN: 1524-4539</identifier><identifier>DOI: 10.1161/01.CIR.94.6.1325</identifier><identifier>PMID: 8822987</identifier><identifier>CODEN: CIRCAZ</identifier><language>eng</language><publisher>Hagerstown, MD: Lippincott Williams & Wilkins</publisher><subject>Aged ; Biological and medical sciences ; Cardiac Output, Low - drug therapy ; Cardiac Output, Low - physiopathology ; Cardiology. Vascular system ; Chemoreceptor Cells - drug effects ; Chemoreceptor Cells - physiology ; Female ; Heart ; Heart failure, cardiogenic pulmonary edema, cardiac enlargement ; Hemodynamics - drug effects ; Humans ; Male ; Medical sciences ; Middle Aged ; Muscles - innervation ; Oxygen - therapeutic use ; Reflex - physiology ; Sympathetic Nervous System - physiopathology</subject><ispartof>Circulation (New York, N.Y.), 1996-09, Vol.94 (6), p.1325-1328</ispartof><rights>1996 INIST-CNRS</rights><rights>Copyright American Heart Association, Inc. Sep 15, 1996</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c323t-e31f966ce18359fafc7c99b89111f75dd23e5884e1882536576d8716792e61623</citedby><cites>FETCH-LOGICAL-c323t-e31f966ce18359fafc7c99b89111f75dd23e5884e1882536576d8716792e61623</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=3218375$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/8822987$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>VAN DE BORNE, P</creatorcontrib><creatorcontrib>OREN, R</creatorcontrib><creatorcontrib>ANDERSON, E. A</creatorcontrib><creatorcontrib>MARK, A. L</creatorcontrib><creatorcontrib>SOMERS, V. K</creatorcontrib><title>Tonic chemoreflex activation does not contribute to elevated muscle sympathetic nerve activity in heart failure</title><title>Circulation (New York, N.Y.)</title><addtitle>Circulation</addtitle><description>Sympathetic activation in heart failure may be due to an increase in sympathetic excitatory influences or to a decrease in inhibitory signals to the brain stem. Chemoreflex sensitivity may be increased in patients with heart failure. The present study tested the hypothesis that tonic activation of excitatory chemoreceptor afferents contributes to the elevated sympathetic activity in heart failure.
We recorded sympathetic nerve activity to muscle circulation from the peroneal nerve of 12 chronic heart failure patients while the patients were breathing room air and during deactivation of the chemoreceptors while the patients were breathing a 100% O2 gas mixture. All patients except 2 were in class III of the New York Heart Association functional classification. Left ventricular ejection fraction defined by radionuclide ventriculography was 24 +/- 2% (mean +/- SE). We also obtained measurements of resting sympathetic nerve activity in 9 healthy control subjects to document that sympathetic nerve activity was elevated in heart failure subjects. Resting sympathetic nerve activity was 59 +/- 5 bursts/min in heart failure patients versus 36 +/- 4 bursts/min in control subjects (P < .01). In heart failure patients, oxygen administration increased oxygen saturation from 94 +/- 0.9% to 99 +/- 0.3% (P < .0001). This increase in oxygen saturation did not affect resting muscle sympathetic nerve activity (798 +/- 122 U/min while patients breathed room air and 824 +/- 35 U/min during 100% O2 breathing) or blood pressure.
Increased efferent sympathetic activity to muscle circulation in patients with heart failure is not explained by tonic activation of excitatory chemoreflex afferents.</description><subject>Aged</subject><subject>Biological and medical sciences</subject><subject>Cardiac Output, Low - drug therapy</subject><subject>Cardiac Output, Low - physiopathology</subject><subject>Cardiology. Vascular system</subject><subject>Chemoreceptor Cells - drug effects</subject><subject>Chemoreceptor Cells - physiology</subject><subject>Female</subject><subject>Heart</subject><subject>Heart failure, cardiogenic pulmonary edema, cardiac enlargement</subject><subject>Hemodynamics - drug effects</subject><subject>Humans</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Middle Aged</subject><subject>Muscles - innervation</subject><subject>Oxygen - therapeutic use</subject><subject>Reflex - physiology</subject><subject>Sympathetic Nervous System - physiopathology</subject><issn>0009-7322</issn><issn>1524-4539</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1996</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpdkUlrHDEQhUVIcCZO7rkERAi5dVtLazuGIYvBEDD2WWjU1YxMtzSR1Mbz7y0zgw85FcX76lFVD6HPlPSUSnpFaL-9vu3N0MuecibeoA0VbOgGwc1btCGEmE5xxt6jD6U8tFZyJS7QhdaMGa02KN2lGDz2e1hShmmGJ-x8DY-uhhTxmKDgmCr2KdYcdmsFXBOGGRoAI17W4mfA5bgcXN1DbU4R8iOcPEI94hDxHlyueHJhXjN8RO8mNxf4dK6X6P7Xz7vtn-7m7-_r7Y-bznPGawecTkZKD1RzYSY3eeWN2WlDKZ2UGEfGQWg9NF0zwaVQctSKSmUYSCoZv0TfT76HnP6tUKpdQvEwzy5CWotVmkvSyAZ-_Q98SGuObTfLKFOMNKxB5AT5nEppf7KHHBaXj5YS-xKEJdS2IKwZrLQvQbSRL2ffdbfA-Dpw_nzTv511V7ybp-yiD-UV46xdrgR_BnYKkLw</recordid><startdate>19960915</startdate><enddate>19960915</enddate><creator>VAN DE BORNE, P</creator><creator>OREN, R</creator><creator>ANDERSON, E. A</creator><creator>MARK, A. L</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>19960915</creationdate><title>Tonic chemoreflex activation does not contribute to elevated muscle sympathetic nerve activity in heart failure</title><author>VAN DE BORNE, P ; OREN, R ; ANDERSON, E. A ; MARK, A. L ; SOMERS, V. K</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c323t-e31f966ce18359fafc7c99b89111f75dd23e5884e1882536576d8716792e61623</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1996</creationdate><topic>Aged</topic><topic>Biological and medical sciences</topic><topic>Cardiac Output, Low - drug therapy</topic><topic>Cardiac Output, Low - physiopathology</topic><topic>Cardiology. Vascular system</topic><topic>Chemoreceptor Cells - drug effects</topic><topic>Chemoreceptor Cells - physiology</topic><topic>Female</topic><topic>Heart</topic><topic>Heart failure, cardiogenic pulmonary edema, cardiac enlargement</topic><topic>Hemodynamics - drug effects</topic><topic>Humans</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Middle Aged</topic><topic>Muscles - innervation</topic><topic>Oxygen - therapeutic use</topic><topic>Reflex - physiology</topic><topic>Sympathetic Nervous System - physiopathology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>VAN DE BORNE, P</creatorcontrib><creatorcontrib>OREN, R</creatorcontrib><creatorcontrib>ANDERSON, E. A</creatorcontrib><creatorcontrib>MARK, A. L</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>VAN DE BORNE, P</au><au>OREN, R</au><au>ANDERSON, E. A</au><au>MARK, A. L</au><au>SOMERS, V. K</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Tonic chemoreflex activation does not contribute to elevated muscle sympathetic nerve activity in heart failure</atitle><jtitle>Circulation (New York, N.Y.)</jtitle><addtitle>Circulation</addtitle><date>1996-09-15</date><risdate>1996</risdate><volume>94</volume><issue>6</issue><spage>1325</spage><epage>1328</epage><pages>1325-1328</pages><issn>0009-7322</issn><eissn>1524-4539</eissn><coden>CIRCAZ</coden><abstract>Sympathetic activation in heart failure may be due to an increase in sympathetic excitatory influences or to a decrease in inhibitory signals to the brain stem. Chemoreflex sensitivity may be increased in patients with heart failure. The present study tested the hypothesis that tonic activation of excitatory chemoreceptor afferents contributes to the elevated sympathetic activity in heart failure.
We recorded sympathetic nerve activity to muscle circulation from the peroneal nerve of 12 chronic heart failure patients while the patients were breathing room air and during deactivation of the chemoreceptors while the patients were breathing a 100% O2 gas mixture. All patients except 2 were in class III of the New York Heart Association functional classification. Left ventricular ejection fraction defined by radionuclide ventriculography was 24 +/- 2% (mean +/- SE). We also obtained measurements of resting sympathetic nerve activity in 9 healthy control subjects to document that sympathetic nerve activity was elevated in heart failure subjects. Resting sympathetic nerve activity was 59 +/- 5 bursts/min in heart failure patients versus 36 +/- 4 bursts/min in control subjects (P < .01). In heart failure patients, oxygen administration increased oxygen saturation from 94 +/- 0.9% to 99 +/- 0.3% (P < .0001). This increase in oxygen saturation did not affect resting muscle sympathetic nerve activity (798 +/- 122 U/min while patients breathed room air and 824 +/- 35 U/min during 100% O2 breathing) or blood pressure.
Increased efferent sympathetic activity to muscle circulation in patients with heart failure is not explained by tonic activation of excitatory chemoreflex afferents.</abstract><cop>Hagerstown, MD</cop><pub>Lippincott Williams & Wilkins</pub><pmid>8822987</pmid><doi>10.1161/01.CIR.94.6.1325</doi><tpages>4</tpages></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 0009-7322 |
| ispartof | Circulation (New York, N.Y.), 1996-09, Vol.94 (6), p.1325-1328 |
| issn | 0009-7322 1524-4539 |
| language | eng |
| recordid | cdi_proquest_miscellaneous_78360616 |
| source | MEDLINE; American Heart Association Journals; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; Journals@Ovid Complete |
| subjects | Aged Biological and medical sciences Cardiac Output, Low - drug therapy Cardiac Output, Low - physiopathology Cardiology. Vascular system Chemoreceptor Cells - drug effects Chemoreceptor Cells - physiology Female Heart Heart failure, cardiogenic pulmonary edema, cardiac enlargement Hemodynamics - drug effects Humans Male Medical sciences Middle Aged Muscles - innervation Oxygen - therapeutic use Reflex - physiology Sympathetic Nervous System - physiopathology |
| title | Tonic chemoreflex activation does not contribute to elevated muscle sympathetic nerve activity in heart failure |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-01-30T01%3A13%3A48IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest_cross&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Tonic%20chemoreflex%20activation%20does%20not%20contribute%20to%20elevated%20muscle%20sympathetic%20nerve%20activity%20in%20heart%20failure&rft.jtitle=Circulation%20(New%20York,%20N.Y.)&rft.au=VAN%20DE%20BORNE,%20P&rft.date=1996-09-15&rft.volume=94&rft.issue=6&rft.spage=1325&rft.epage=1328&rft.pages=1325-1328&rft.issn=0009-7322&rft.eissn=1524-4539&rft.coden=CIRCAZ&rft_id=info:doi/10.1161/01.CIR.94.6.1325&rft_dat=%3Cproquest_cross%3E78360616%3C/proquest_cross%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=212720606&rft_id=info:pmid/8822987&rfr_iscdi=true |