Linked Life Data

6086177

Source:http://linkedlifedata.com/resource/pubmed/id/6086177

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
1984-9-14
pubmed:abstractText
The present study was performed to clarify oxygen-induced damage following myocardial reperfusion, using three mitochondrial preparations from isolated rabbit hearts (nonischemic hearts and those subjected to 40 and 90 minutes of normothermic global ischemia). The viability of mitochondria was evaluated by adenosine triphosphate generation. The extent of mitochondrial injury produced by reactive oxygen metabolism was assessed by the intensity of hydroxyl radical signal detected with electron spin resonance spectroscopy and the reduction of coenzyme Q10 level. The greatest oxygen-induced injury was observed in 40-minute ischemic mitochondria exposed to pure oxygen. The use of superoxide dismutase and catalase satisfactorily prevented the oxygen-induced injury. Moreover, the net adenosine triphosphate generation of the 40-minute ischemic mitochondria was comparable to that of the nonischemic mitochondria without the enzymes. These results suggest that reperfusion of the ischemic myocardium with viable mitochondria is deleterious, because mitochondria are susceptible to injury resulting from oxidative metabolism, and that the use of superoxide dismutase, together with catalase, is beneficial for the restoration of cardiac function after ischemia.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Aug
pubmed:issn
0009-7330
pubmed:author
pubmed:issnType
Print
pubmed:volume
55
pubmed:owner
NLM
pubmed:authorsComplete
N
pubmed:pagination
168-75
pubmed:dateRevised
2007-11-15
pubmed:meshHeading
pubmed:year
1984
pubmed:articleTitle
In vitro study on contribution of oxidative metabolism of isolated rabbit heart mitochondria to myocardial reperfusion injury.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't