Linked Life Data

10222030

Source:http://linkedlifedata.com/resource/pubmed/id/10222030

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3
pubmed:dateCreated
1999-7-13
pubmed:abstractText
We have investigated the pathophysiological basis of cardiac dysfunction in autoimmune myocarditis and in the resulting dilated cardiomyopathy. To this end we utilized the myosin-induced autoimmune myocarditis model in BALB/c mice. Myocarditis has been found to be associated with massive ventricular lymphocyte infiltration and a 50% reduction in tail artery blood flow, reflecting the depressed cardiac function in myocarditis. Action potential characteristics of control and diseased isolated ventricular myocytes were (mean+/-SEM): resting potential: -68.1+/-1. 1,-68.3+/-0.7 mV; action potential amplitude: 96.5+/-10.4, 92.3+/-4. 4 mV; action potential duration at 80% repolarization (APD80) 38+/-5, 116+/-24* ms; * P<0.05. We utilized the whole cell voltage clamp technique to explore ion currents involved in APD prolongation and arrhythmogenic activity, and found that in diseased myocytes the transient outward current (Ito) was markedly attenuated. At a membrane potential of +40 mV, in control and in diseased myocytes, I(to) current density was 14.7+/-1.5 and 6.5+/-1.4 pA/pF, respectively, P<0.005. In contrast, the L-type Ca2+current (ICa,L) remained unchanged. To further explore the basis for cardiac impairment, we simultaneously measured [Ca2+]i transient and contraction in isolated normal and diseased myocytes. The major findings indicated that both the relaxation kinetics of [Ca2+]i transients and myocyte contraction were significantly faster in the diseased myocytes. In conclusion, substantial, potentially reversible, electrophysiological and mechanical perturbations in ventricular myocytes from mice with myosin-induced autoimmune myocarditis appear to contribute to disease-related cardiac dysfunction.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
May
pubmed:issn
0896-8411
pubmed:author
pubmed:copyrightInfo
Copyright 1999 Academic Press.
pubmed:issnType
Print
pubmed:volume
12
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
209-20
pubmed:dateRevised
2009-11-19
pubmed:meshHeading
pubmed-meshheading:10222030-Action Potentials, pubmed-meshheading:10222030-Animals, pubmed-meshheading:10222030-Autoantigens, pubmed-meshheading:10222030-Autoimmune Diseases, pubmed-meshheading:10222030-Calcium Channels, pubmed-meshheading:10222030-Calcium Channels, L-Type, pubmed-meshheading:10222030-Calcium Signaling, pubmed-meshheading:10222030-Cardiomyopathy, Dilated, pubmed-meshheading:10222030-Cells, Cultured, pubmed-meshheading:10222030-Electric Conductivity, pubmed-meshheading:10222030-Heart Function Tests, pubmed-meshheading:10222030-Heart Ventricles, pubmed-meshheading:10222030-Mice, pubmed-meshheading:10222030-Mice, Inbred BALB C, pubmed-meshheading:10222030-Muscle Proteins, pubmed-meshheading:10222030-Myocardial Contraction, pubmed-meshheading:10222030-Myocarditis, pubmed-meshheading:10222030-Myocardium, pubmed-meshheading:10222030-Myosins, pubmed-meshheading:10222030-T-Lymphocytes, Cytotoxic
pubmed:year
1999
pubmed:articleTitle
Cardiac dysfunction in murine autoimmune myocarditis.
pubmed:affiliation
Rappaport Family Institute for Research in the Medical Sciences, Bruce Rappaport Faculty of Medicine, The Bernard Katz Minerva Center for Cell Biophysics, Technion-Israel Institute of Technology, Haifa, 31096, Israel.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't