Linked Life Data

9038957

Source:http://linkedlifedata.com/resource/pubmed/id/9038957

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1 Pt 2
pubmed:dateCreated
1997-3-31
pubmed:abstractText
To determine whether myocardial infarction leads to alterations in myofilament isometric tension as a function of Ca2+ concentration, unloaded shortening velocity, and sarcomere compliance, these properties were examined in skinned myocytes 7 days after coronary artery occlusion. Changes in myofilament proteins were also evaluated Myocardial infarction was characterized by a 10-15% reduction in myofilament isometric tension at submaximum Ca2+ levels in the physiological range. However, developed tension at maximum activation was unaltered. Conversely, unloaded shortening velocity was decreased by 31% in the remaining viable cells, whereas resting tension was increased by 30-40%. The regulatory protein troponin I content was reduced, but phosphorylation of troponin I and troponin T was increased. Myosin isoenzymes and troponin T contents were not altered. In conclusion, molecular responses occurred acutely after myocardial infarction, and these adaptations may depress the mechanical behavior of the unaffected cells, contributing to acute impairment in global cardiac pump function beyond that resulting from myocyte loss.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jan
pubmed:issn
0002-9513
pubmed:author
pubmed:issnType
Print
pubmed:volume
272
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
H360-70
pubmed:dateRevised
2011-11-17
pubmed:meshHeading
pubmed:year
1997
pubmed:articleTitle
Myocardial infarction alters myofilament calcium sensitivity and mechanical behavior of myocytes.
pubmed:affiliation
Department of Medicine, New York Medical College, Valhalla 10595, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't