Linked Life Data

7503262

Source:http://linkedlifedata.com/resource/pubmed/id/7503262

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
5 Pt 2
pubmed:dateCreated
1996-1-17
pubmed:abstractText
In diabetes a primary myocardial defect occurs that is characterized by decreases in systolic pressure and cardiac output. The present study investigates whether diabetes causes a decreased maximum tension-generating ability, decreased Ca2+ sensitivity of myofilaments, or no change in cardiac myofilament contractile properties at pH 7.0 and 6.6. Hearts from Wistar rats were excised and mechanically disrupted 6-10 wk after injection of streptozotocin. The resulting myocyte-size preparations of skinned myocardium were used to determine the steady-state tension-negative, log molar Ca2+ concentration (pCa) relation. Maximum tension was unchanged, and the pCa of half-maximum tension generation was 0.14 pCa units lower than control for skinned myocytes from diabetic rats at pH 7.0. A significantly lower than normal maximum tension was observed at pH 6.6 for cardiac myocytes from diabetic rats. Increased expression of beta-myosin heavy chain (MHC) occurred in hearts from diabetic rats. Two troponin T (TnT) isoforms in myocardium of adult rats were identified by Western blots. The ratio of the two TnT isoforms were altered in diabetes. Changes in cardiac MHC and TnT expression may contribute to the observed decrease in Ca2+ sensitivity of myofilaments at pH 7.0 and decreased maximum tension-generating ability at pH 6.6 in diabetes.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Nov
pubmed:issn
0002-9513
pubmed:author
pubmed:issnType
Print
pubmed:volume
269
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
H1656-63
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed:year
1995
pubmed:articleTitle
Effects of diabetes on isometric tension as a function of [Ca2+] and pH in rat skinned cardiac myocytes.
pubmed:affiliation
Department of Physiology and Biophysics, University of Tennessee, Memphis 38163, USA.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't