Behavior of expiratory neurons in response to mechanical and chemical loading
The response of medullary expiratory neurons to added mechanical and chemical loads was studied in anesthetized cats. Alterations in burst characteristics and central timing were compared in the intact and bilaterally vagotomized cat. The following results were obtained: (1) Graded expiratory airflo...
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Veröffentlicht in: | Respiration physiology 1979-01, Vol.36 (3), p.337-351 |
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description | The response of medullary expiratory neurons to added mechanical and chemical loads was studied in anesthetized cats. Alterations in burst characteristics and central timing were compared in the intact and bilaterally vagotomized cat. The following results were obtained:
(1) Graded expiratory airflow resistances caused progressive increase in burst duration, spikes per burst and firing rate; similar effects were noted for end-inspiratory tracheal occlusions and continuous positive pressure breathing; all facilitation was eliminated by vagotomy.
(2) Graded inspiratory airflow resistances delayed the onset of an expiratory burst but did not change the overall burst characteristics.
(3) Acute hypercapnia increased ventilation without noticeable changes in expiratory burst characteristics; acute hypoxia produced a reduction in burst duration concomitant with changes in ventilation.
It is concluded that (1) expiratory neurons are responsive to vagally mediated volume information and (2) transient hypoxia and hypercapnia sufficient to increase ventilation does not increase the firing rate of expiratory neurons but exerts differential effects with respect to timing. It is suggested that expiratory duration is related to the time integral of expired volume and that the increase in FRC imposed by expiratory loads does not alter the central timing of the next inspiration. |
doi_str_mv | 10.1016/0034-5687(79)90046-X |
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(1) Graded expiratory airflow resistances caused progressive increase in burst duration, spikes per burst and firing rate; similar effects were noted for end-inspiratory tracheal occlusions and continuous positive pressure breathing; all facilitation was eliminated by vagotomy.
(2) Graded inspiratory airflow resistances delayed the onset of an expiratory burst but did not change the overall burst characteristics.
(3) Acute hypercapnia increased ventilation without noticeable changes in expiratory burst characteristics; acute hypoxia produced a reduction in burst duration concomitant with changes in ventilation.
It is concluded that (1) expiratory neurons are responsive to vagally mediated volume information and (2) transient hypoxia and hypercapnia sufficient to increase ventilation does not increase the firing rate of expiratory neurons but exerts differential effects with respect to timing. It is suggested that expiratory duration is related to the time integral of expired volume and that the increase in FRC imposed by expiratory loads does not alter the central timing of the next inspiration.</description><identifier>ISSN: 0034-5687</identifier><identifier>DOI: 10.1016/0034-5687(79)90046-X</identifier><identifier>PMID: 441585</identifier><language>eng</language><publisher>Netherlands: Elsevier B.V</publisher><subject>Action Potentials ; Airway Obstruction - physiopathology ; Animals ; Cats ; Control of breathing ; Hypercapnia ; Hypercapnia - physiopathology ; Hypoxia ; Hypoxia - physiopathology ; Medulla Oblongata - physiology ; Pressure breathing ; Respiration ; Respiratory centers ; Space life sciences ; Tracheal occlusion</subject><ispartof>Respiration physiology, 1979-01, Vol.36 (3), p.337-351</ispartof><rights>1979</rights><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c451t-eeeda6281d387368a4a0970135cfb22fe445ba37fc2990e0f8858c2f2261ef513</citedby><cites>FETCH-LOGICAL-c451t-eeeda6281d387368a4a0970135cfb22fe445ba37fc2990e0f8858c2f2261ef513</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,777,781,27905,27906</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/441585$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Baker, J.P.</creatorcontrib><creatorcontrib>Frazier, D.T.</creatorcontrib><creatorcontrib>Hanley, M.</creatorcontrib><creatorcontrib>Zechman, F.W.</creatorcontrib><title>Behavior of expiratory neurons in response to mechanical and chemical loading</title><title>Respiration physiology</title><addtitle>Respir Physiol</addtitle><description>The response of medullary expiratory neurons to added mechanical and chemical loads was studied in anesthetized cats. Alterations in burst characteristics and central timing were compared in the intact and bilaterally vagotomized cat. The following results were obtained:
(1) Graded expiratory airflow resistances caused progressive increase in burst duration, spikes per burst and firing rate; similar effects were noted for end-inspiratory tracheal occlusions and continuous positive pressure breathing; all facilitation was eliminated by vagotomy.
(2) Graded inspiratory airflow resistances delayed the onset of an expiratory burst but did not change the overall burst characteristics.
(3) Acute hypercapnia increased ventilation without noticeable changes in expiratory burst characteristics; acute hypoxia produced a reduction in burst duration concomitant with changes in ventilation.
It is concluded that (1) expiratory neurons are responsive to vagally mediated volume information and (2) transient hypoxia and hypercapnia sufficient to increase ventilation does not increase the firing rate of expiratory neurons but exerts differential effects with respect to timing. It is suggested that expiratory duration is related to the time integral of expired volume and that the increase in FRC imposed by expiratory loads does not alter the central timing of the next inspiration.</description><subject>Action Potentials</subject><subject>Airway Obstruction - physiopathology</subject><subject>Animals</subject><subject>Cats</subject><subject>Control of breathing</subject><subject>Hypercapnia</subject><subject>Hypercapnia - physiopathology</subject><subject>Hypoxia</subject><subject>Hypoxia - physiopathology</subject><subject>Medulla Oblongata - physiology</subject><subject>Pressure breathing</subject><subject>Respiration</subject><subject>Respiratory centers</subject><subject>Space life sciences</subject><subject>Tracheal occlusion</subject><issn>0034-5687</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1979</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kMtOwzAQRb3gXfiDLrxCsAjYiZ3HBgkqXlIRG5C6s1xnTI0SO9hJRf-epKm6ZDVzZ-ZeaQ5CU0puKKHpLSEJi3iaZ1dZcV0QwtJocYBO9-MTdBbCN-l1StJjdMQY5Tk_RW8PsJJr4zx2GsNvY7xsnd9gC513NmBjsYfQ9C3g1uEa1Epao2SFpS2xWkG9FZWTpbFf5-hQyyrAxa5O0OfT48fsJZq_P7_O7ueRYpy2EQCUMo1zWiZ5lqS5ZJIUGaEJV3oZxxoY40uZZFrFRUGA6DznuYp1HKcUNKfJBF2OuY13Px2EVtQmKKgqacF1QWSMkyRjwyEbD5V3IXjQovGmln4jKBEDODEQEgMhkRViC04sett0l98tayj3ppFav74b19D_uDbgRVAGrILSeFCtKJ35P_8Py6N_PQ</recordid><startdate>19790101</startdate><enddate>19790101</enddate><creator>Baker, J.P.</creator><creator>Frazier, D.T.</creator><creator>Hanley, M.</creator><creator>Zechman, F.W.</creator><general>Elsevier B.V</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>19790101</creationdate><title>Behavior of expiratory neurons in response to mechanical and chemical loading</title><author>Baker, J.P. ; Frazier, D.T. ; Hanley, M. ; Zechman, F.W.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c451t-eeeda6281d387368a4a0970135cfb22fe445ba37fc2990e0f8858c2f2261ef513</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1979</creationdate><topic>Action Potentials</topic><topic>Airway Obstruction - physiopathology</topic><topic>Animals</topic><topic>Cats</topic><topic>Control of breathing</topic><topic>Hypercapnia</topic><topic>Hypercapnia - physiopathology</topic><topic>Hypoxia</topic><topic>Hypoxia - physiopathology</topic><topic>Medulla Oblongata - physiology</topic><topic>Pressure breathing</topic><topic>Respiration</topic><topic>Respiratory centers</topic><topic>Space life sciences</topic><topic>Tracheal occlusion</topic><toplevel>online_resources</toplevel><creatorcontrib>Baker, J.P.</creatorcontrib><creatorcontrib>Frazier, D.T.</creatorcontrib><creatorcontrib>Hanley, M.</creatorcontrib><creatorcontrib>Zechman, F.W.</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>Respiration physiology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Baker, J.P.</au><au>Frazier, D.T.</au><au>Hanley, M.</au><au>Zechman, F.W.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Behavior of expiratory neurons in response to mechanical and chemical loading</atitle><jtitle>Respiration physiology</jtitle><addtitle>Respir Physiol</addtitle><date>1979-01-01</date><risdate>1979</risdate><volume>36</volume><issue>3</issue><spage>337</spage><epage>351</epage><pages>337-351</pages><issn>0034-5687</issn><abstract>The response of medullary expiratory neurons to added mechanical and chemical loads was studied in anesthetized cats. Alterations in burst characteristics and central timing were compared in the intact and bilaterally vagotomized cat. The following results were obtained:
(1) Graded expiratory airflow resistances caused progressive increase in burst duration, spikes per burst and firing rate; similar effects were noted for end-inspiratory tracheal occlusions and continuous positive pressure breathing; all facilitation was eliminated by vagotomy.
(2) Graded inspiratory airflow resistances delayed the onset of an expiratory burst but did not change the overall burst characteristics.
(3) Acute hypercapnia increased ventilation without noticeable changes in expiratory burst characteristics; acute hypoxia produced a reduction in burst duration concomitant with changes in ventilation.
It is concluded that (1) expiratory neurons are responsive to vagally mediated volume information and (2) transient hypoxia and hypercapnia sufficient to increase ventilation does not increase the firing rate of expiratory neurons but exerts differential effects with respect to timing. It is suggested that expiratory duration is related to the time integral of expired volume and that the increase in FRC imposed by expiratory loads does not alter the central timing of the next inspiration.</abstract><cop>Netherlands</cop><pub>Elsevier B.V</pub><pmid>441585</pmid><doi>10.1016/0034-5687(79)90046-X</doi><tpages>15</tpages></addata></record> |
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subjects | Action Potentials Airway Obstruction - physiopathology Animals Cats Control of breathing Hypercapnia Hypercapnia - physiopathology Hypoxia Hypoxia - physiopathology Medulla Oblongata - physiology Pressure breathing Respiration Respiratory centers Space life sciences Tracheal occlusion |
title | Behavior of expiratory neurons in response to mechanical and chemical loading |
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