Please use this identifier to cite or link to this item: http://ahro.austin.org.au/austinjspui/handle/1/12897
Title: Reperfusion-induced calcium gain after ischemia.
Authors: Elz, J S;Panagiotopoulos, Sianna;Nayler, W G
Affiliation: Department of Medicine, University of Melbourne, Austin Hospital, Heidelberg, Victoria, Australia.
Issue Date: 7-Mar-1989
Citation: The American Journal of Cardiology; 63(10): 7E-13E
Abstract: Reperfusion-induced calcium gain provides a marker of irreversible injury, but whether the cells gain calcium because of irreversible injury caused by the ischemic episode, or whether it is the reperfusion-induced calcium gain that triggers the irreversible injury has yet to be established. Using isolated rat hearts made ischemic for either 30 or 60 minutes, and reperfusing with Krebs-Henseleit buffer or Krebs-Henseleit buffer containing either 2,3-butanedione monoxime (to inhibit contractile activity) or 2,4-dinitrophenol or nitrogen-gassed substrate-free Krebs-Henseleit buffer (to inhibit oxidative phosphorylation), the effect of reperfusion was monitored in terms of calcium gain and ultrastructural changes including loss of sarcolemmal integrity. The results establish that the routes of calcium entry during postischemic reperfusion are complex. The calcium gain can occur in the absence of mitochondrial oxidative phosphorylation and is modulated by interventions introduced at the moment of reperfusion which affect the contractile state. There are at least 2 routes of calcium entry: contraction-dependent and contraction independent. The former is probably associated with the development of sarcolemmal discontinuities. The results also establish that when sarcolemmal integrity has been destroyed, the cells can gain excess calcium under conditions that prevent mitochondrial calcium uptake. Accordingly, the mitochondria cannot be the only intracellular organelles that accumulate calcium under these conditions. Additional studies are needed to identify the other sites of calcium binding under conditions of adenosine triphosphate deprivation.
Internal ID Number: 2923053
URI: http://ahro.austin.org.au/austinjspui/handle/1/12897
ORCID: 0000-0002-0845-0001
URL: http://www.ncbi.nlm.nih.gov/pubmed/2923053
Type: Journal Article
Subjects: 2,4-Dinitrophenol
Animals
Calcium.metabolism
Coronary Disease.metabolism.therapy
Dinitrophenols.pharmacology
Epoxy Compounds.pharmacology
In Vitro Techniques
Myocardial Contraction.drug effects
Myocardial Reperfusion Injury.metabolism
Oxidative Phosphorylation.drug effects
Rats
Rats, Inbred Strains
Sarcolemma.ultrastructure
Appears in Collections:Journal articles

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