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dc.contributor.authorFenton, Richard A.
dc.contributor.authorDobson, James G. Jr.
dc.date2022-08-11T08:10:16.000
dc.date.accessioned2022-08-23T17:02:00Z
dc.date.available2022-08-23T17:02:00Z
dc.date.issued1993-03-01
dc.date.submitted2008-06-09
dc.identifier.citationCirc Res. 1993 Mar;72(3):571-8.
dc.identifier.issn0009-7330 (Print)
dc.identifier.pmid8381722
dc.identifier.urihttp://hdl.handle.net/20.500.14038/44130
dc.description.abstractEndogenous interstitial adenosine may protect the hypoxic heart by attenuating beta-adrenergic-induced contractile and metabolic responses, thereby reducing energy utilization. Constant-flow perfused rat hearts were used to study: 1) the effect of hypoxia on isoproterenol (ISO)-induced increase in interstitial adenosine, as estimated with epicardial surface transudates, and 2) the role of endogenous adenosine in hypoxic depression of ISO-induced contractile responses. ISO (1 nM for 10 minutes) in the normoxic heart increased transudate adenosine 114% from a pre-ISO normoxic value of 343 pmol/ml. ISO administered to the hypoxic heart increased transudate adenosine 357% from a pre-ISO hypoxic value of 797 pmol/ml. The absolute magnitude of the ISO-induced increase in transudate adenosine was 625% greater during hypoxia than during normoxia. This was associated with a reduction in the ISO-induced contractile response during hypoxia. In other experiments, with normoxia ISO (10 nM for 10 seconds) increased developed left ventricular pressure by 140 mm Hg, and the maximum rates of left ventricular pressure development and relaxation by 5,860 and 2,771 mm Hg/sec, respectively, above control values of 90 mm Hg, 2,250 mm Hg/sec, and 1,875 mm Hg/sec. Hypoxia reduced the three ISO-induced contractile responses by 50%, 56%, and 36%. However, 1,3-dipropyl-8-cyclopentylxanthine (5 x 10(-7) M), an adenosine A1-receptor antagonist, added to the hypoxic hearts resulted in only a 31%, 39%, and 9% reduction in the ISO-induced responses in developed left ventricular pressure and the maximum rates of left ventricular pressure development and relaxation, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)
dc.language.isoen_US
dc.relation<a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8381722&dopt=Abstract ">Link to article in PubMed</a>
dc.relation.urlhttp://circres.ahajournals.org/content/72/3/571.long
dc.subjectAdenosine
dc.subjectAnimals
dc.subjectCell Hypoxia
dc.subjectDisease Models, Animal
dc.subjectHeart
dc.subjectIsoproterenol
dc.subjectMale
dc.subjectMyocardial Contraction
dc.subjectMyocardial Ischemia
dc.subjectOxygen Consumption
dc.subjectRats
dc.subjectRats, Sprague-Dawley
dc.subjectReceptors, Adrenergic, beta
dc.subjectCardiovascular Diseases
dc.subjectNervous System Diseases
dc.subjectPhysiology
dc.titleHypoxia enhances isoproterenol-induced increase in heart interstitial adenosine, depressing beta-adrenergic contractile responses
dc.typeJournal Article
dc.source.journaltitleCirculation research
dc.source.volume72
dc.source.issue3
dc.identifier.legacycoverpagehttps://escholarship.umassmed.edu/physio_pp/12
dc.identifier.contextkey521864
html.description.abstract<p>Endogenous interstitial adenosine may protect the hypoxic heart by attenuating beta-adrenergic-induced contractile and metabolic responses, thereby reducing energy utilization. Constant-flow perfused rat hearts were used to study: 1) the effect of hypoxia on isoproterenol (ISO)-induced increase in interstitial adenosine, as estimated with epicardial surface transudates, and 2) the role of endogenous adenosine in hypoxic depression of ISO-induced contractile responses. ISO (1 nM for 10 minutes) in the normoxic heart increased transudate adenosine 114% from a pre-ISO normoxic value of 343 pmol/ml. ISO administered to the hypoxic heart increased transudate adenosine 357% from a pre-ISO hypoxic value of 797 pmol/ml. The absolute magnitude of the ISO-induced increase in transudate adenosine was 625% greater during hypoxia than during normoxia. This was associated with a reduction in the ISO-induced contractile response during hypoxia. In other experiments, with normoxia ISO (10 nM for 10 seconds) increased developed left ventricular pressure by 140 mm Hg, and the maximum rates of left ventricular pressure development and relaxation by 5,860 and 2,771 mm Hg/sec, respectively, above control values of 90 mm Hg, 2,250 mm Hg/sec, and 1,875 mm Hg/sec. Hypoxia reduced the three ISO-induced contractile responses by 50%, 56%, and 36%. However, 1,3-dipropyl-8-cyclopentylxanthine (5 x 10(-7) M), an adenosine A1-receptor antagonist, added to the hypoxic hearts resulted in only a 31%, 39%, and 9% reduction in the ISO-induced responses in developed left ventricular pressure and the maximum rates of left ventricular pressure development and relaxation, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)</p>
dc.identifier.submissionpathphysio_pp/12
dc.contributor.departmentDepartment of Physiology
dc.source.pages571-8


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