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Article: Influence of stimulation parameters on the release of adenosine, lactate and CO2 from contracting dog gracilis muscle

TitleInfluence of stimulation parameters on the release of adenosine, lactate and CO2 from contracting dog gracilis muscle
Authors
Issue Date1993
PublisherWiley-Blackwell Publishing Ltd.. The Journal's web site is located at http://www.wiley.com/bw/journal.asp?ref=0022-3751
Citation
Journal Of Physiology, 1993, v. 463, p. 107-121 How to Cite?
Abstract1. The addition of adenosine, CO2 and lactate to the venous blood draining an isolated constant-flow perfused gracilis muscle was studied in anaesthetized and artificially ventilated dogs during twitch and tetanic contractions. 2. Venous adenosine concentration increased from 154 ± 33 nM (mean ± S.E.M.) to 279 ± 121 or 280 ± 125 nM after 10 min of 1.5 or 3 Hz twitch contractions and to 240 ± 120 or 276 ± 139 nM after 10 min of 1 or 5 s tetani occurring at 0.1 Hz. Twitch contractions at 0.1 or 0.5 Hz for 10 min did not significantly elevate venous adenosine. 3. Venous lactate concentration was significantly increased after 10 min of 1.5 or 3 Hz twitches or 5 s tetani at 0.1 Hz. There was a good correlation (r = 0.70; P < 0.001) between venous adenosine and lactate concentrations. 4. Venous partial pressure of CO2 (P(CO2)) was significantly elevated after 10 min of 1.5 or 3 Hz twitch contractions or 1 or 5 s tetani at 0.1 Hz. There was also a good correlation (r = 0.58; P < 0.001) between venous adenosine concentration and P(CO2). 5. Venous partial pressure Of O2 (P(O2)) decreased during all contractions except those at 0.1 Hz, but the oxygen cost per unit of tension x time was similar during every pattern of stimulation, and the percentage of the total energy production achieved by anaerobic means during muscle contractions did not exceed that at rest, indicating that there had been no limitation to the oxygen supply. Venous P(O2) was poorly correlated with venous adenosine concentration (r = 0.28), but quite well correlated with venous lactate concentration (r = 0.53; P < 0.001). If the indirect influence of P(O2) on venous adenosine concentration via an increase in lactate concentration was eliminated by partial correlation, then the coefficient for the relationship between venous adenosine concentration and venous P(O2) became 0.15. 6. There was a significant correlation between the venous adenosine concentration and the venous pH (r = 0.53; P < 0.001). If the influence of oxygenation on venous adenosine and pH was eliminated by partial correlation, the coefficient for the relationship between venous adenosine and pH increased to 0.95. 7. These data support a role for pH in the control of adenosine release from skeletal muscle, and confirm that the amounts of lactate released during muscle contractions were large enough to have caused the adenosine release. Adenosine output did not appear to be directly related to muscle oxygenation, but an indirect association whereby oxygen lack stimulated lactate production, and lactate in turn stimulated azdenosine production remains possible.
Persistent Identifierhttp://hdl.handle.net/10722/171587
ISSN
2015 Impact Factor: 4.731
2015 SCImago Journal Rankings: 2.670
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorAchike, FIen_US
dc.contributor.authorBallard, HJen_US
dc.date.accessioned2012-10-30T06:15:50Z-
dc.date.available2012-10-30T06:15:50Z-
dc.date.issued1993en_US
dc.identifier.citationJournal Of Physiology, 1993, v. 463, p. 107-121en_US
dc.identifier.issn0022-3751en_US
dc.identifier.urihttp://hdl.handle.net/10722/171587-
dc.description.abstract1. The addition of adenosine, CO2 and lactate to the venous blood draining an isolated constant-flow perfused gracilis muscle was studied in anaesthetized and artificially ventilated dogs during twitch and tetanic contractions. 2. Venous adenosine concentration increased from 154 ± 33 nM (mean ± S.E.M.) to 279 ± 121 or 280 ± 125 nM after 10 min of 1.5 or 3 Hz twitch contractions and to 240 ± 120 or 276 ± 139 nM after 10 min of 1 or 5 s tetani occurring at 0.1 Hz. Twitch contractions at 0.1 or 0.5 Hz for 10 min did not significantly elevate venous adenosine. 3. Venous lactate concentration was significantly increased after 10 min of 1.5 or 3 Hz twitches or 5 s tetani at 0.1 Hz. There was a good correlation (r = 0.70; P < 0.001) between venous adenosine and lactate concentrations. 4. Venous partial pressure of CO2 (P(CO2)) was significantly elevated after 10 min of 1.5 or 3 Hz twitch contractions or 1 or 5 s tetani at 0.1 Hz. There was also a good correlation (r = 0.58; P < 0.001) between venous adenosine concentration and P(CO2). 5. Venous partial pressure Of O2 (P(O2)) decreased during all contractions except those at 0.1 Hz, but the oxygen cost per unit of tension x time was similar during every pattern of stimulation, and the percentage of the total energy production achieved by anaerobic means during muscle contractions did not exceed that at rest, indicating that there had been no limitation to the oxygen supply. Venous P(O2) was poorly correlated with venous adenosine concentration (r = 0.28), but quite well correlated with venous lactate concentration (r = 0.53; P < 0.001). If the indirect influence of P(O2) on venous adenosine concentration via an increase in lactate concentration was eliminated by partial correlation, then the coefficient for the relationship between venous adenosine concentration and venous P(O2) became 0.15. 6. There was a significant correlation between the venous adenosine concentration and the venous pH (r = 0.53; P < 0.001). If the influence of oxygenation on venous adenosine and pH was eliminated by partial correlation, the coefficient for the relationship between venous adenosine and pH increased to 0.95. 7. These data support a role for pH in the control of adenosine release from skeletal muscle, and confirm that the amounts of lactate released during muscle contractions were large enough to have caused the adenosine release. Adenosine output did not appear to be directly related to muscle oxygenation, but an indirect association whereby oxygen lack stimulated lactate production, and lactate in turn stimulated azdenosine production remains possible.en_US
dc.languageengen_US
dc.publisherWiley-Blackwell Publishing Ltd.. The Journal's web site is located at http://www.wiley.com/bw/journal.asp?ref=0022-3751en_US
dc.relation.ispartofJournal of Physiologyen_US
dc.subject.meshAdenosine - Metabolismen_US
dc.subject.meshAnimalsen_US
dc.subject.meshAnoxia - Metabolismen_US
dc.subject.meshBlood Gas Analysisen_US
dc.subject.meshCarbon Dioxide - Blood - Metabolismen_US
dc.subject.meshDogsen_US
dc.subject.meshElectric Stimulationen_US
dc.subject.meshHemodynamics - Physiologyen_US
dc.subject.meshHydrogen-Ion Concentrationen_US
dc.subject.meshLactates - Blood - Metabolismen_US
dc.subject.meshLactic Aciden_US
dc.subject.meshMuscle Contraction - Physiologyen_US
dc.subject.meshMuscles - Metabolismen_US
dc.subject.meshOxygen Consumption - Physiologyen_US
dc.subject.meshPerfusionen_US
dc.subject.meshVascular Resistance - Physiologyen_US
dc.titleInfluence of stimulation parameters on the release of adenosine, lactate and CO2 from contracting dog gracilis muscleen_US
dc.typeArticleen_US
dc.identifier.emailBallard, HJ:ballard@hkucc.hku.hken_US
dc.identifier.authorityBallard, HJ=rp00367en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.pmid8246177-
dc.identifier.scopuseid_2-s2.0-0027413588en_US
dc.identifier.volume463en_US
dc.identifier.spage107en_US
dc.identifier.epage121en_US
dc.identifier.isiWOS:A1993KW77900006-
dc.publisher.placeUnited Kingdomen_US
dc.identifier.scopusauthoridAchike, FI=6701844593en_US
dc.identifier.scopusauthoridBallard, HJ=7005286310en_US

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