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Article: Acute systemic hypoxia elevates venous but not interstitial potassium of dog skeletal muscle

TitleAcute systemic hypoxia elevates venous but not interstitial potassium of dog skeletal muscle
Authors
Issue Date2005
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, 2005, v. 289 n. 4 58-4, p. H1710-H1718 How to Cite?
AbstractPotassium release through ATP-sensitive potassium (KATP) channels contributes to hypoxic vasodilation in the skeletal muscle vascular bed: It is uncertain whether KATP channels on muscle cells contribute to the process. Potassium from muscle cells must cross the interstitial space to reach the vascular tissues, whereas that from vascular endothelium would have a higher concentration in venous blood than in interstitial fluid. We determined the effect of systemic hypoxia on arterial, venous, and interstitial potassium in the constant-flow-perfused gracilis muscles of anesthetized dogs. Hypoxia reduced arterial PO2 from 138 to 25 and PCO2 from 28 to 26 mmHg. Arterial pH and potassium were well correlated (r2 = 0.9): Both increased in early hypoxia and decreased during the postcontrol. In denervated muscles, perfusion pressure decreased from 95 to 76 mmHg by the end of the hypoxic period; neither venous nor interstitial potassium was elevated. In innervated muscles, perfusion pressure increased from 110 to 172 mmHg by the 11th min of hypoxia and then decreased to 146 mmHg by the end of the hypoxic period; venous potassium increased from 5.0 to 5.3 mM, but interstitial potassium remained unchanged. Glibenclamide abolished both the increase in venous potassium and the hypoxic vasodilation in the innervated muscle. Thus skeletal muscle cells were unlikely to have contributed to the release of potassium, which was suggested to originate from vascular endothelium. The sympathetic nerve supply may play a direct or indirect role in the opening of KATP channels under hypoxic conditions. Copyright © 2005 the American Physiological Society.
Persistent Identifierhttp://hdl.handle.net/10722/81181
ISSN
2015 Impact Factor: 3.324
2015 SCImago Journal Rankings: 1.823
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorMo, FMen_HK
dc.contributor.authorBallard, HJen_HK
dc.date.accessioned2010-09-06T08:14:45Z-
dc.date.available2010-09-06T08:14:45Z-
dc.date.issued2005en_HK
dc.identifier.citationAmerican Journal Of Physiology - Heart And Circulatory Physiology, 2005, v. 289 n. 4 58-4, p. H1710-H1718en_HK
dc.identifier.issn0363-6135en_HK
dc.identifier.urihttp://hdl.handle.net/10722/81181-
dc.description.abstractPotassium release through ATP-sensitive potassium (KATP) channels contributes to hypoxic vasodilation in the skeletal muscle vascular bed: It is uncertain whether KATP channels on muscle cells contribute to the process. Potassium from muscle cells must cross the interstitial space to reach the vascular tissues, whereas that from vascular endothelium would have a higher concentration in venous blood than in interstitial fluid. We determined the effect of systemic hypoxia on arterial, venous, and interstitial potassium in the constant-flow-perfused gracilis muscles of anesthetized dogs. Hypoxia reduced arterial PO2 from 138 to 25 and PCO2 from 28 to 26 mmHg. Arterial pH and potassium were well correlated (r2 = 0.9): Both increased in early hypoxia and decreased during the postcontrol. In denervated muscles, perfusion pressure decreased from 95 to 76 mmHg by the end of the hypoxic period; neither venous nor interstitial potassium was elevated. In innervated muscles, perfusion pressure increased from 110 to 172 mmHg by the 11th min of hypoxia and then decreased to 146 mmHg by the end of the hypoxic period; venous potassium increased from 5.0 to 5.3 mM, but interstitial potassium remained unchanged. Glibenclamide abolished both the increase in venous potassium and the hypoxic vasodilation in the innervated muscle. Thus skeletal muscle cells were unlikely to have contributed to the release of potassium, which was suggested to originate from vascular endothelium. The sympathetic nerve supply may play a direct or indirect role in the opening of KATP channels under hypoxic conditions. Copyright © 2005 the American Physiological Society.en_HK
dc.languageengen_HK
dc.publisherAmerican Physiological Society. The Journal's web site is located at http://intl-ajpheart.physiology.org/en_HK
dc.relation.ispartofAmerican Journal of Physiology - Heart and Circulatory Physiologyen_HK
dc.titleAcute systemic hypoxia elevates venous but not interstitial potassium of dog skeletal muscleen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0363-6135&volume=289&spage=H1710&epage=H1718&date=2005&atitle=Acute+systemic+hypoxia+elevates+venous+but+not+interstitial+potassium+of+dog+skeletal+muscleen_HK
dc.identifier.emailBallard, HJ: ballard@hkucc.hku.hken_HK
dc.identifier.authorityBallard, HJ=rp00367en_HK
dc.description.naturelink_to_OA_fulltext-
dc.identifier.doi10.1152/ajpheart.00614.2004en_HK
dc.identifier.pmid15894574-
dc.identifier.scopuseid_2-s2.0-25444506579en_HK
dc.identifier.hkuros107431en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-25444506579&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume289en_HK
dc.identifier.issue4 58-4en_HK
dc.identifier.spageH1710en_HK
dc.identifier.epageH1718en_HK
dc.identifier.isiWOS:000231875300047-
dc.publisher.placeUnited Statesen_HK
dc.identifier.scopusauthoridMo, FM=7005059536en_HK
dc.identifier.scopusauthoridBallard, HJ=7005286310en_HK

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