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Article: The effect of systemic hypoxia on interstitial and blood adenosine, AMP, ADP and ATP in dog skeletal muscle

TitleThe effect of systemic hypoxia on interstitial and blood adenosine, AMP, ADP and ATP in dog skeletal muscle
Authors
Issue Date2001
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, 2001, v. 536 n. 2, p. 593-603 How to Cite?
Abstract1. We investigated the effect of moderate systemic hypoxia on the arterial, venous and interstitial concentration of adenosine and adenine nucleotides in the neurally and vascularly isolated, constant-flow perfused gracilis muscles of anaesthetized dogs. 2. Systemic hypoxia reduced arterial P O2 from 129 to 28 mm Hg, venous P O2 from 63 to 23 mmHg, arterial pH from 7.43 to 7.36 and venous pH from 7.38 to 7.32. Neither arterial nor venous P CO2 were changed. Arterial perfusion pressure remained at 109 ± 8 mmHg for the first 5 min of hypoxia, then increased to 131 ± 11 mmHg by 9 min, and then decreased again throughout the rest of the hypoxic period. 3. Arterial adenosine (427 ± 98 nM) did not change during hypoxia, but venous adenosine increased from 350 ± 52 to 518 ± 107 nM. Interstitial adenosine concentration did not increase (339 ± 154 nM in normoxia and 262 ± 97 nM in hypoxia). Neither arterial nor venous nor interstitial concentrations of adenine nucleotides changed significantly in hypoxia. 4. Interstitial adenosine, AMP, ADP and ATP increased from 194 ± 40, 351 ± 19, 52 ± 7 and 113 ± 36 to 764 ± 140, 793 ± 119, 403 ± 67 and 574 ± 122 nM, respectively, during 2 Hz muscle contractions. 5. Adenosine, AMP, ADP and ATP infused into the arterial blood did not elevate the interstitial concentration until the arterial concentration exceeded 10 μM. 6. We conclude that the increased adenosine in skeletal muscle during systemic hypoxia is formed by the vascular tissue or the blood cells, and that adenosine is formed intracellularly by these tissues. On the other hand, adenosine formation takes place extracellularly in the interstitial space during muscle contractions.
Persistent Identifierhttp://hdl.handle.net/10722/49304
ISSN
2015 Impact Factor: 4.731
2015 SCImago Journal Rankings: 2.670
PubMed Central ID
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorMo, FMen_HK
dc.contributor.authorBallard, HJen_HK
dc.date.accessioned2008-06-12T06:38:56Z-
dc.date.available2008-06-12T06:38:56Z-
dc.date.issued2001en_HK
dc.identifier.citationJournal Of Physiology, 2001, v. 536 n. 2, p. 593-603en_HK
dc.identifier.issn0022-3751en_HK
dc.identifier.urihttp://hdl.handle.net/10722/49304-
dc.description.abstract1. We investigated the effect of moderate systemic hypoxia on the arterial, venous and interstitial concentration of adenosine and adenine nucleotides in the neurally and vascularly isolated, constant-flow perfused gracilis muscles of anaesthetized dogs. 2. Systemic hypoxia reduced arterial P O2 from 129 to 28 mm Hg, venous P O2 from 63 to 23 mmHg, arterial pH from 7.43 to 7.36 and venous pH from 7.38 to 7.32. Neither arterial nor venous P CO2 were changed. Arterial perfusion pressure remained at 109 ± 8 mmHg for the first 5 min of hypoxia, then increased to 131 ± 11 mmHg by 9 min, and then decreased again throughout the rest of the hypoxic period. 3. Arterial adenosine (427 ± 98 nM) did not change during hypoxia, but venous adenosine increased from 350 ± 52 to 518 ± 107 nM. Interstitial adenosine concentration did not increase (339 ± 154 nM in normoxia and 262 ± 97 nM in hypoxia). Neither arterial nor venous nor interstitial concentrations of adenine nucleotides changed significantly in hypoxia. 4. Interstitial adenosine, AMP, ADP and ATP increased from 194 ± 40, 351 ± 19, 52 ± 7 and 113 ± 36 to 764 ± 140, 793 ± 119, 403 ± 67 and 574 ± 122 nM, respectively, during 2 Hz muscle contractions. 5. Adenosine, AMP, ADP and ATP infused into the arterial blood did not elevate the interstitial concentration until the arterial concentration exceeded 10 μM. 6. We conclude that the increased adenosine in skeletal muscle during systemic hypoxia is formed by the vascular tissue or the blood cells, and that adenosine is formed intracellularly by these tissues. On the other hand, adenosine formation takes place extracellularly in the interstitial space during muscle contractions.en_HK
dc.format.extent388 bytes-
dc.format.mimetypetext/html-
dc.languageengen_HK
dc.publisherWiley-Blackwell Publishing Ltd.. The Journal's web site is located at http://www.wiley.com/bw/journal.asp?ref=0022-3751en_HK
dc.relation.ispartofJournal of Physiologyen_HK
dc.rightsThe Journal of Physiology. Copyright © Blackwell Publishing Ltd.en_HK
dc.rightsCreative Commons: Attribution 3.0 Hong Kong License-
dc.rightsThe definitive version is available at www.blackwell-synergy.comen_HK
dc.subject.meshAdenine Nucleotides - blooden_HK
dc.subject.meshAnoxia - blooden_HK
dc.subject.meshMuscle, Skeletal - blood supply - metabolismen_HK
dc.subject.meshAdenosine Diphosphate - blooden_HK
dc.subject.meshAdenosine Monophosphate - blooden_HK
dc.titleThe effect of systemic hypoxia on interstitial and blood adenosine, AMP, ADP and ATP in dog skeletal muscleen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0022-3751&volume=536&issue=2&spage=593&epage=603&date=2001&atitle=The+effect+of+systemic+hypoxia+on+interstitial+and+blood+adenosine,+AMP,+ADP+and+ATP+in+dog+skeletal+muscleen_HK
dc.identifier.emailBallard, HJ: ballard@hkucc.hku.hken_HK
dc.identifier.authorityBallard, HJ=rp00367en_HK
dc.description.naturepublished_or_final_versionen_HK
dc.identifier.doi10.1111/j.1469-7793.2001.0593c.xden_HK
dc.identifier.pmid11600692-
dc.identifier.pmcidPMC2278877en_HK
dc.identifier.scopuseid_2-s2.0-0035887271en_HK
dc.identifier.hkuros72902-
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-0035887271&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume536en_HK
dc.identifier.issue2en_HK
dc.identifier.spage593en_HK
dc.identifier.epage603en_HK
dc.identifier.isiWOS:000171807700024-
dc.publisher.placeUnited Kingdomen_HK
dc.identifier.scopusauthoridMo, FM=7005059536en_HK
dc.identifier.scopusauthoridBallard, HJ=7005286310en_HK

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