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Article: Intracellular lactate controls adenosine output from dog gracilis muscle during moderate systemic hypoxia

TitleIntracellular lactate controls adenosine output from dog gracilis muscle during moderate systemic hypoxia
Authors
KeywordsΑ-Cyano-4-Hydroxycinnamic Acid
Canine
Red Muscle
Issue Date1997
PublisherAmerican Physiological Society. The Journal's web site is located at http://intl-ajpheart.physiology.org/
Citation
American Journal Of Physiology - Heart And Circulatory Physiology, 1997, v. 272 n. 1 41-1, p. H318-H324 How to Cite?
AbstractThe influence of systemic hypoxia on lactate and adenosine output from isolated constant-flow-perfused gracilis muscle was determined in anesthetized dogs. The lactate transport inhibitor α-cyano-4-hydroxycinnamic acid (CHCA) was employed to distinguish the direct effects of hypoxia on adenosine output from the effects produced indirectly by a change in lactate concentration. Reduction of arterial PO2 from 135 ± 4 to 39 ± 2 mmHg raised arterial lactate from 1.26 ± 0.32 to 2.22 ± 0.45 mM but decreased venoarterial lactate difference from 0.53 ± 0.09 to -0.13 ± 0.19 mM, indicating that lactate output from the muscle was abolished. Arterial adenosine did not change, but venoarterial adenosine difference increased from 20.6 ± 10.1 to 76.5 ± 14.4 nM. CHCA infusion during hypoxia abolished adenosine output from gracilis muscle (venoarterial adenosine difference = - 20.5 ± 40.6 nM). In isolated rat soleus muscle fibers, intracellular pH increased from 6.96 ± 0.04 to 7.71 ± 0.14 in response to a reduction of PO2 from 459 ± 28 to 53 ± 3 mmHg. Correspondingly, adenosine output decreased from 3.71 ± 0.15 to 3.04 ± 0.27 nM. These data suggest that hypoxia did not directly stimulate adenosine output from red oxidative skeletal muscle, but rather systemic hypoxia increased lactate delivery and the resulting increase in intracellular lactate decreased intracellular pH, which stimulated adenosine output.
Persistent Identifierhttp://hdl.handle.net/10722/171640
ISSN
2015 Impact Factor: 3.324
2015 SCImago Journal Rankings: 1.823
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorMo, FMen_US
dc.contributor.authorBallard, HJen_US
dc.date.accessioned2012-10-30T06:16:06Z-
dc.date.available2012-10-30T06:16:06Z-
dc.date.issued1997en_US
dc.identifier.citationAmerican Journal Of Physiology - Heart And Circulatory Physiology, 1997, v. 272 n. 1 41-1, p. H318-H324en_US
dc.identifier.issn0363-6135en_US
dc.identifier.urihttp://hdl.handle.net/10722/171640-
dc.description.abstractThe influence of systemic hypoxia on lactate and adenosine output from isolated constant-flow-perfused gracilis muscle was determined in anesthetized dogs. The lactate transport inhibitor α-cyano-4-hydroxycinnamic acid (CHCA) was employed to distinguish the direct effects of hypoxia on adenosine output from the effects produced indirectly by a change in lactate concentration. Reduction of arterial PO2 from 135 ± 4 to 39 ± 2 mmHg raised arterial lactate from 1.26 ± 0.32 to 2.22 ± 0.45 mM but decreased venoarterial lactate difference from 0.53 ± 0.09 to -0.13 ± 0.19 mM, indicating that lactate output from the muscle was abolished. Arterial adenosine did not change, but venoarterial adenosine difference increased from 20.6 ± 10.1 to 76.5 ± 14.4 nM. CHCA infusion during hypoxia abolished adenosine output from gracilis muscle (venoarterial adenosine difference = - 20.5 ± 40.6 nM). In isolated rat soleus muscle fibers, intracellular pH increased from 6.96 ± 0.04 to 7.71 ± 0.14 in response to a reduction of PO2 from 459 ± 28 to 53 ± 3 mmHg. Correspondingly, adenosine output decreased from 3.71 ± 0.15 to 3.04 ± 0.27 nM. These data suggest that hypoxia did not directly stimulate adenosine output from red oxidative skeletal muscle, but rather systemic hypoxia increased lactate delivery and the resulting increase in intracellular lactate decreased intracellular pH, which stimulated adenosine output.en_US
dc.languageengen_US
dc.publisherAmerican Physiological Society. The Journal's web site is located at http://intl-ajpheart.physiology.org/en_US
dc.relation.ispartofAmerican Journal of Physiology - Heart and Circulatory Physiologyen_US
dc.subjectΑ-Cyano-4-Hydroxycinnamic Acid-
dc.subjectCanine-
dc.subjectRed Muscle-
dc.subject.meshAdenosine - Blood - Metabolismen_US
dc.subject.meshAnimalsen_US
dc.subject.meshAnoxia - Blood - Metabolism - Physiopathologyen_US
dc.subject.meshDogsen_US
dc.subject.meshGases - Blooden_US
dc.subject.meshHemodynamicsen_US
dc.subject.meshHindlimben_US
dc.subject.meshHydrogen-Ion Concentrationen_US
dc.subject.meshIntracellular Fluid - Metabolismen_US
dc.subject.meshIntracellular Membranes - Metabolismen_US
dc.subject.meshLactic Acid - Blood - Metabolismen_US
dc.subject.meshMaleen_US
dc.subject.meshMuscle, Skeletal - Metabolismen_US
dc.subject.meshOsmolar Concentrationen_US
dc.subject.meshRatsen_US
dc.subject.meshRats, Sprague-Dawleyen_US
dc.titleIntracellular lactate controls adenosine output from dog gracilis muscle during moderate systemic hypoxiaen_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.pmid9038952-
dc.identifier.scopuseid_2-s2.0-0031013199en_US
dc.identifier.hkuros27886-
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-0031013199&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume272en_US
dc.identifier.issue1 41-1en_US
dc.identifier.spageH318en_US
dc.identifier.epageH324en_US
dc.identifier.isiWOS:A1997WG57200037-
dc.publisher.placeUnited Statesen_US
dc.identifier.scopusauthoridMo, FM=7005059536en_US
dc.identifier.scopusauthoridBallard, HJ=7005286310en_US

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