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DC Field | Value | Language |
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dc.contributor.author | Nayler, W G | en |
dc.date.accessioned | 2015-05-15T23:43:36Z | |
dc.date.available | 2015-05-15T23:43:36Z | |
dc.date.issued | 1991-05-16 | en |
dc.identifier.citation | Journal of Cardiovascular Pharmacology; 18 Suppl 6(): S10-4 | en |
dc.identifier.govdoc | 1725910 | en |
dc.identifier.other | PUBMED | en |
dc.identifier.uri | https://ahro.austin.org.au/austinjspui/handle/1/10312 | en |
dc.description.abstract | The 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.iso | en | en |
dc.subject.other | Adenosine Triphosphate.metabolism | en |
dc.subject.other | Animals | en |
dc.subject.other | Calcium.metabolism | en |
dc.subject.other | Calcium Channel Blockers.pharmacology | en |
dc.subject.other | Coronary Disease.metabolism | en |
dc.subject.other | Cytosol.metabolism | en |
dc.subject.other | Male | en |
dc.subject.other | Myocardial Reperfusion | en |
dc.subject.other | Myocardium.metabolism | en |
dc.subject.other | Phosphocreatine.metabolism | en |
dc.subject.other | Rats | en |
dc.subject.other | Rats, Inbred Strains | en |
dc.subject.other | Verapamil.pharmacology | en |
dc.title | Cardioprotective aspects of calcium antagonists. | en |
dc.type | Journal Article | en |
dc.identifier.journaltitle | Journal of Cardiovascular Pharmacology | en |
dc.identifier.affiliation | Department of Medicine, University of Melbourne, Austin Hospital, Heidelberg, Australia | en |
dc.description.pages | S10-4 | en |
dc.relation.url | https://pubmed.ncbi.nlm.nih.gov/1725910 | en |
dc.type.austin | Journal Article | en |
item.openairecristype | http://purl.org/coar/resource_type/c_18cf | - |
item.cerifentitytype | Publications | - |
item.fulltext | No Fulltext | - |
item.grantfulltext | none | - |
item.languageiso639-1 | en | - |
item.openairetype | Journal Article | - |
Appears in Collections: | Journal articles |
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