help button home button Am J Pathol ASIP MEMBERSHIP
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS

This Article
Right arrow Order Full text via Infotrieve
Services
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow reprints & permissions
Citing Articles
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Ashraf, M.
Right arrow Articles by Bloor, C. M.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Ashraf, M.
Right arrow Articles by Bloor, C. M.

American Journal of Pathology, Vol 90, 423-434, Copyright © 1978 by American Society for Investigative Pathology


REGULAR ARTICLES

Ultrastructural influence of reperfusing dog myocardium with calcium- free blood after coronary artery occlusion

M Ashraf, F White and CM Bloor

The ultrastructural effects of perfusing ischemic myocardium with calcium-free blood were determined in 12 dogs. In 6 dogs, the left anterior descending coronary artery was ligated for 45 minutes and was released for 5, 10, or 20 minutes. In 6 other dogs, the ischemic zone was perfused with blood free of calcium which was chelated with EGTA (ethylene glycol bis [B-aminoethylether-N,N'-tetraacetic acid] for 5, 10, or 20 minutes. After reperfusion with whole blood, the sarcomeres either were mildly contracted or formed contracted bands. The cells were usually pulled apart at the intercalated disk. The mitochondria were swollen and contained electron-dense deposits. Lanthanum was used as a marker for monitoring changes in cell membrane permeability and permeated into many ischemic myocardial cells. The hearts treated with calcium-free plasma showed well preserved morphology. Mitochondria were slightly swollen, their cristae were occasionally disrupted, and they lacked electron-dense deposits. No lanthanum leaked into these cells, with a few scattered exceptions. Even in the leaky cells, the mitochondria did not show any deposits. It is suggested that calcium overload plays a significant role in the pathogenesis of cell injury and that reduction in plasma levels of calcium, at least for a limited period may delay the onset of calcium overload and improve cell morphology. Alterations in the cell membrane are followed by lethal intracellular changes leading to events associated with cell death.





HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Copyright © 1978 by the American Society for Investigative Pathology.