Linked Life Data

6994187

Source:http://linkedlifedata.com/resource/pubmed/id/6994187

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:dateCreated
1980-9-28
pubmed:abstractText
Hypoxia and anoxia were induced in isolated perfused rat hearts by reduction of perfusate oxygen. Ischemia was produced by restricting coronary flow in hearts working against high resistance. Protein degradation, estimated from release of phenylalanine into the perfusate in the presence of cycloheximide, was inhibited in both anoxic and ischemia as compared to aerobic hearts. The effect of ischemia was greater than that of anoxia. A similar inhibitory effect was observed in energy-poor hearts when insulin was present in the perfusate. Other experiments indicated that the effects of energy depletion were exerted at a step early in the degradative pathway, since peptide products of partial proteolysis did not accumulate. A graded reduction in perfusate oxygen tension (hypoxia) led to a significant inhibition of proteolysis with unaltered tissue levels of nucleotides and creatine phosphate. Protein degradation was inhibited in aerobic and anoxic hearts exposed to increasing extracellular levels of hydrogen ions and lactate, suggesting that reduced proteolysis in hearts that are provided limited oxygen may result from accumulation of metabolites as well as from energy depletion per se.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:issn
0270-4056
pubmed:author
pubmed:issnType
Print
pubmed:volume
1
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
535-46
pubmed:dateRevised
2011-11-17
pubmed:meshHeading
pubmed:year
1980
pubmed:articleTitle
Inhibition of protein degradation in the energy-poor heart.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S.