Please use this identifier to cite or link to this item: https://ahro.austin.org.au/austinjspui/handle/1/12969
Full metadata record
DC FieldValueLanguage
dc.contributor.authorNayler, W Gen
dc.contributor.authorElz, J Sen
dc.contributor.authorBuckley, D Jen
dc.date.accessioned2015-05-16T02:44:12Z
dc.date.available2015-05-16T02:44:12Z
dc.date.issued1988-04-01en
dc.identifier.citationThe American Journal of Physiology; 254(4 Pt 2): H678-85en
dc.identifier.govdoc3354696en
dc.identifier.otherPUBMEDen
dc.identifier.urihttps://ahro.austin.org.au/austinjspui/handle/1/12969en
dc.description.abstractWhen isolated hearts are perfused with substrate-free hypoxic buffer for prolonged periods of time, resting tension and tissue Ca increase. These two events may be interrelated. Isolated rat hearts were used to establish whether the hypoxia-induced increase in tissue Ca can be dissociated from the rise in resting tension. Tension generation was inhibited at the start of hypoxic perfusion by adding 2,3-butanedione monoxime (BDM, 30 mM). In other experiments the Ca2+ in the hypoxic buffer was reduced from 1.3 to 0.1 mM. After 30-120 min of hypoxia, ventricular muscle was assayed for ATP, creatine phosphate, Ca, and Na, and the perfusion defect was established. Resting tension was recorded before and throughout the hypoxic perfusion. Sixty minutes of perfusion with 1.3 mM Ca2+ glucose-free hypoxic buffer caused the tissue Ca to increase (P less than 0.01). Resting tension increased by 7.9 +/- 0.6 g (P less than 0.01). Sixty minutes of perfusion with 0.1 mM Ca2+ glucose-free hypoxic buffer failed to cause an increase in tissue Ca, but resting tension increased (P less than 0.01). During perfusion with glucose-free hypoxic buffer containing 2.6 mM Ca2+ and 30 mM BDM, resting tension remained low for up to 120 min, but after 60 min Ca accumulation occurred. After 120 min of BDM-hypoxic perfusion, tissue Ca reached 11.8 +/- 0.9 mumol/g dry wt. With or without BDM, hypoxia caused an early increase in tissue Na ahead of any increase in tissue Ca.(ABSTRACT TRUNCATED AT 250 WORDS)en
dc.language.isoenen
dc.subject.otherAdenosine Triphosphate.metabolismen
dc.subject.otherAerobiosisen
dc.subject.otherAnaerobiosisen
dc.subject.otherAnimalsen
dc.subject.otherAnoxia.physiopathologyen
dc.subject.otherCalcium.metabolismen
dc.subject.otherEpoxy Compounds.pharmacologyen
dc.subject.otherFemaleen
dc.subject.otherHeart.drug effects.physiology.physiopathologyen
dc.subject.otherHeart Ventricles.metabolismen
dc.subject.otherIn Vitro Techniquesen
dc.subject.otherMyocardium.metabolismen
dc.subject.otherPerfusionen
dc.subject.otherPhosphocreatine.metabolismen
dc.subject.otherRatsen
dc.subject.otherRats, Inbred Strainsen
dc.subject.otherSodium.metabolismen
dc.titleDissociation of hypoxia-induced calcium gain and rise in resting tension in isolated rat hearts.en
dc.typeJournal Articleen
dc.identifier.journaltitleAmerican Journal of Physiologyen
dc.identifier.affiliationDepartment of Medicine, University of Melbourne, Austin Hospital, Heidelberg, Victoria, Australiaen
dc.description.pagesH678-85en
dc.relation.urlhttps://pubmed.ncbi.nlm.nih.gov/3354696en
dc.type.austinJournal Articleen
item.openairecristypehttp://purl.org/coar/resource_type/c_18cf-
item.cerifentitytypePublications-
item.fulltextNo Fulltext-
item.grantfulltextnone-
item.languageiso639-1en-
item.openairetypeJournal Article-
Appears in Collections:Journal articles
Show simple item record

Page view(s)

2
checked on Mar 28, 2024

Google ScholarTM

Check


Items in AHRO are protected by copyright, with all rights reserved, unless otherwise indicated.