Document Detail


Ischemia induces early changes to cytoskeletal and contractile proteins in diseased human myocardium.
MedLine Citation:
PMID:  7609573     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Ischemia is known to produce damage to subcellular organelles, such as nuclei and mitochondria, in myocardial tissue. We tested the hypothesis that during myocardial ischemia various cytoskeletal and contractile proteins also undergo changes. We induced total global ischemia by incubation in buffer of tissue samples from six human left ventricles that were obtained from heart transplant recipients. Samples were removed from the incubation medium at different time intervals and investigated by immunohistochemistry using monoclonal antibodies against myosin, actin, tropomyosin, troponin T, myomesin, desmin, tubulin, and vinculin. The degree of ischemic injury was determined by electron microscopy. Ischemic cardiomyopathic human tissue showed disturbances of the localization pattern of myosin, actin, tropomyosin, and troponin T as early as 10 minutes after the onset of ischemia; this disruption was complete at 20 minutes. Tubulin also started changing at 10 minutes, but complete disruption was only evident after 120 minutes. Desmin and myomesin showed an intermediate response; changes began at 30 to 40 minutes, and disruption was complete at 90 to 120 minutes. Vinculin was most resistant to ischemia. Ultrastructurally, the tissue showed moderate reversible ischemic injury during the entire period of 180 minutes. Measuring the exposure time in seconds allowed quantitation of the intensity of the fluorescence. We reached the following conclusions: (1) Ischemia causes damage to the contractile proteins sooner than to the cytoskeleton and subcellular organelles. (2) Diseased human hearts are extremely susceptible to the effects of ischemia. These findings are important for the situation of induced cardiac arrest in heart operations and for preservation of donor hearts for transplantation.
Authors:
S Hein; T Scheffold; J Schaper
Related Documents :
6969163 - Salvage of acutely ischemic myocardium by emergency coronary artery bypass grafting.
23228563 - Ventricular activity morphological characterization: ectopic beats removal in long term...
3518093 - Accidental severe hypothermia.
Publication Detail:
Type:  In Vitro; Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  The Journal of thoracic and cardiovascular surgery     Volume:  110     ISSN:  0022-5223     ISO Abbreviation:  J. Thorac. Cardiovasc. Surg.     Publication Date:  1995 Jul 
Date Detail:
Created Date:  1995-08-11     Completed Date:  1995-08-11     Revised Date:  2009-11-19    
Medline Journal Info:
Nlm Unique ID:  0376343     Medline TA:  J Thorac Cardiovasc Surg     Country:  UNITED STATES    
Other Details:
Languages:  eng     Pagination:  89-98     Citation Subset:  AIM; IM    
Affiliation:
Max-Planck-Institute for Physiological and Clinical Research, Department of Experimental Cardiology, Bad Nauheim, Germany.
Export Citation:
APA/MLA Format     Download EndNote     Download BibTex
MeSH Terms
Descriptor/Qualifier:
Actins / analysis
Biological Markers / analysis
Blotting, Western
Cell Nucleus / ultrastructure
Contractile Proteins / ultrastructure*
Cytoskeleton / ultrastructure*
Desmin / analysis
Humans
Microscopy, Electron
Microscopy, Fluorescence
Muscle Proteins / analysis
Myocardial Ischemia / pathology*
Myocardium / ultrastructure*
Myosins / analysis
Organelles / ultrastructure*
Tropomyosin / analysis
Troponin / analysis
Troponin T
Tubulin / analysis
Vinculin / analysis
Chemical
Reg. No./Substance:
0/Actins; 0/Biological Markers; 0/Contractile Proteins; 0/Desmin; 0/Muscle Proteins; 0/Tropomyosin; 0/Troponin; 0/Troponin T; 0/Tubulin; 0/myomesin; 125361-02-6/Vinculin; EC 3.6.4.1/Myosins

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


Previous Document:  Ultrastructural changes during continuous retrograde warm and mild hypothermic blood cardioplegia fo...
Next Document:  Interleukin-8 and monocyte chemotactic activating factor responses to cardiopulmonary bypass.