Please use this identifier to cite or link to this item: https://ahro.austin.org.au/austinjspui/handle/1/10312
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dc.contributor.authorNayler, W Gen
dc.date.accessioned2015-05-15T23:43:36Z
dc.date.available2015-05-15T23:43:36Z
dc.date.issued1991-05-16en
dc.identifier.citationJournal of Cardiovascular Pharmacology; 18 Suppl 6(): S10-4en
dc.identifier.govdoc1725910en
dc.identifier.otherPUBMEDen
dc.identifier.urihttps://ahro.austin.org.au/austinjspui/handle/1/10312en
dc.description.abstractThe use of calcium antagonists as cardioprotective agents is based on the assumption that uncontrolled Ca2+ gain is a key factor in causing cell death and tissue necrosis. This uncontrolled gain in Ca2+ is the ultimate expression of a series of metabolic events triggered by inadequate perfusion. One of the early events is a rise in cytosolic Ca2+ (Cai2+). Using 1,2-bis(e-amino-5-fluorophenoxy)ethan-N1N1N11N11tetraacetic acid and nuclear magnetic resonance spectroscopy to monitor this early rise in Cai2+, it is possible to show that, in isolated perfused rat hearts, Cai2+ increases (p less than 0.01) within the initial 10 min of ischemia and that the increase progresses with time. Possible causes of this early rise in Cai2+ include activation of the endothelin-1 receptors with the subsequent inositol triphosphate-induced activation of sarcoplasmic (SR) Ca2+ release, enhanced Ca(2+)-induced Ca2+ release from the SR reticulum, displacement of bound Ca2+ by the accumulating protons and entry of Ca2+ in exchange for Na+, or through the voltage-sensitive Ca2+ channels. Using the d and l isomers of verapamil it is possible to show that verapamil slows the early rise in Cai2+, the l isomer being more effective (p less than 0.01) than the d isomer. This, in addition to its established energy-sparing effect, may contribute to the effectiveness of verapamil as a cardioprotective agent when used prophylactically.en
dc.language.isoenen
dc.subject.otherAdenosine Triphosphate.metabolismen
dc.subject.otherAnimalsen
dc.subject.otherCalcium.metabolismen
dc.subject.otherCalcium Channel Blockers.pharmacologyen
dc.subject.otherCoronary Disease.metabolismen
dc.subject.otherCytosol.metabolismen
dc.subject.otherMaleen
dc.subject.otherMyocardial Reperfusionen
dc.subject.otherMyocardium.metabolismen
dc.subject.otherPhosphocreatine.metabolismen
dc.subject.otherRatsen
dc.subject.otherRats, Inbred Strainsen
dc.subject.otherVerapamil.pharmacologyen
dc.titleCardioprotective aspects of calcium antagonists.en
dc.typeJournal Articleen
dc.identifier.journaltitleJournal of Cardiovascular Pharmacologyen
dc.identifier.affiliationDepartment of Medicine, University of Melbourne, Austin Hospital, Heidelberg, Australiaen
dc.description.pagesS10-4en
dc.relation.urlhttps://pubmed.ncbi.nlm.nih.gov/1725910en
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-
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