File Download

There are no files associated with this item.

  Links for fulltext
     (May Require Subscription)
Supplementary

Article: The influence of lactic acid on adenosine release from skeletal muscle in anaesthetized dogs

TitleThe influence of lactic acid on adenosine release from skeletal muscle in anaesthetized dogs
Authors
Issue Date1991
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, 1991, v. 433, p. 95-108 How to Cite?
AbstractIn anaesthetized and artificially ventilated dogs, a gracilis muscle was vascularly isolated and perfused at a constant flow rate of 11.9 ± 2.2 ml min-1 100 g-1 (mean ± S.E.M., n = 16; equivalent to 170.2 ± 21.3% of its resting free flow). Stimulation (3 Hz) of the obturator nerve produced twitch contractions of the gracilis muscle, reduced venous pH from 7.366 ± 0.027 to 7.250 ± 0.031 (n = 5), increased oxygen consumption from 0.62 ± 0.24 to 2.76 ± 0.46 ml min-1 100 g-1 (n = 5) and increased adenosine release from -0.40 ± 0.14 (net uptake) to 1.36 ± 0.50 nmol min-1 100 g-1 (n = 8). Infusion of lactic acid (4.2 mM) into the artery reduced venous pH to 7.281 ± 0.026 (n = 5) and increased adenosine release to 0.96 ± 0.40 nmol min-1 100 g-1 (n = 8), but did not significantly alter oxygen consumption (0.80 ± 0.19 ml min-1 100 g-1; n = 5). Stimulation (3 Hz) in the presence of lactic acid infusion produced no further significant changes in venous pH or adenosine release, but increased oxygen consumption to 2.53 ± 0.37 ml min-1 100 g-1 (n = 5). Infusion of a range of lactic acid concentrations (≥ 1.83 mM) produced dose-dependent increases in adenosine release. The maximum lactic acid concentration tested (5.95 mM) reduced venous pH to 7.249 ± 0.023 (n = 5) and increased adenosine release to 2.64 ± 1.26 nmol min-1 100 g-1 (n = 6). A strong correlation existed between the adenosine release and the venous pH (r = -0.92); points obtained during muscle stimulation and/or lactic acid infusion fell on a single correlation line. The vasoactivity of adenosine administered by close-arterial injection was unaltered by infusion of either lactic acid (7.2 mM) or saline. These results suggest that the release of adenosine from skeletal muscle can be induced by a decrease in pH (probably at an intracellular site), and that this mechanism may contribute to the release of adenosine during muscle contractions.
Persistent Identifierhttp://hdl.handle.net/10722/171560
ISSN
2015 Impact Factor: 4.731
2015 SCImago Journal Rankings: 2.670
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorBallard, HJen_US
dc.date.accessioned2012-10-30T06:15:41Z-
dc.date.available2012-10-30T06:15:41Z-
dc.date.issued1991en_US
dc.identifier.citationJournal Of Physiology, 1991, v. 433, p. 95-108en_US
dc.identifier.issn0022-3751en_US
dc.identifier.urihttp://hdl.handle.net/10722/171560-
dc.description.abstractIn anaesthetized and artificially ventilated dogs, a gracilis muscle was vascularly isolated and perfused at a constant flow rate of 11.9 ± 2.2 ml min-1 100 g-1 (mean ± S.E.M., n = 16; equivalent to 170.2 ± 21.3% of its resting free flow). Stimulation (3 Hz) of the obturator nerve produced twitch contractions of the gracilis muscle, reduced venous pH from 7.366 ± 0.027 to 7.250 ± 0.031 (n = 5), increased oxygen consumption from 0.62 ± 0.24 to 2.76 ± 0.46 ml min-1 100 g-1 (n = 5) and increased adenosine release from -0.40 ± 0.14 (net uptake) to 1.36 ± 0.50 nmol min-1 100 g-1 (n = 8). Infusion of lactic acid (4.2 mM) into the artery reduced venous pH to 7.281 ± 0.026 (n = 5) and increased adenosine release to 0.96 ± 0.40 nmol min-1 100 g-1 (n = 8), but did not significantly alter oxygen consumption (0.80 ± 0.19 ml min-1 100 g-1; n = 5). Stimulation (3 Hz) in the presence of lactic acid infusion produced no further significant changes in venous pH or adenosine release, but increased oxygen consumption to 2.53 ± 0.37 ml min-1 100 g-1 (n = 5). Infusion of a range of lactic acid concentrations (≥ 1.83 mM) produced dose-dependent increases in adenosine release. The maximum lactic acid concentration tested (5.95 mM) reduced venous pH to 7.249 ± 0.023 (n = 5) and increased adenosine release to 2.64 ± 1.26 nmol min-1 100 g-1 (n = 6). A strong correlation existed between the adenosine release and the venous pH (r = -0.92); points obtained during muscle stimulation and/or lactic acid infusion fell on a single correlation line. The vasoactivity of adenosine administered by close-arterial injection was unaltered by infusion of either lactic acid (7.2 mM) or saline. These results suggest that the release of adenosine from skeletal muscle can be induced by a decrease in pH (probably at an intracellular site), and that this mechanism may contribute to the release of adenosine during muscle contractions.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 - Blood - Secretionen_US
dc.subject.meshAnimalsen_US
dc.subject.meshDogsen_US
dc.subject.meshDose-Response Relationship, Drugen_US
dc.subject.meshElectric Stimulationen_US
dc.subject.meshGases - Blooden_US
dc.subject.meshHemodynamics - Drug Effectsen_US
dc.subject.meshHydrogen-Ion Concentrationen_US
dc.subject.meshInfusions, Intra-Arterialen_US
dc.subject.meshLactates - Administration & Dosage - Pharmacologyen_US
dc.subject.meshLactic Aciden_US
dc.subject.meshMuscle Contraction - Physiologyen_US
dc.subject.meshMuscles - Drug Effects - Physiology - Secretionen_US
dc.titleThe influence of lactic acid on adenosine release from skeletal muscle in anaesthetized dogsen_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.pmid1841964-
dc.identifier.scopuseid_2-s2.0-0026090324en_US
dc.identifier.volume433en_US
dc.identifier.spage95en_US
dc.identifier.epage108en_US
dc.identifier.isiWOS:A1991EW69400006-
dc.publisher.placeUnited Kingdomen_US
dc.identifier.scopusauthoridBallard, HJ=7005286310en_US

Export via OAI-PMH Interface in XML Formats


OR


Export to Other Non-XML Formats