help button home button Am J Pathol The FASEB Journal
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 HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Borgers, M.
Right arrow Articles by Van Overloop, P.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Borgers, M.
Right arrow Articles by Van Overloop, P.

American Journal of Pathology, Vol 126, 92-102, Copyright © 1987 by American Society for Investigative Pathology


REGULAR ARTICLES

Changes in ultrastructure and Ca2+ distribution in the isolated working rabbit heart after ischemia. A time-related study

M Borgers, LG Shu, R Xhonneux, F Thone and P Van Overloop

Ultrastructural changes in cardiac muscle of isolated working rabbit hearts after various periods of ischemia are described and compared with distributional changes in calcium. The effects of reperfusion on these structural parameters were also investigated. The purposes of this study were to relate the role of calcium in the degeneration of cardiac muscle; to determine whether Ca2+ localizations could serve as additional criteria to determine more closely the point of no return; and to investigate the contributory role of reoxygenation to the development of myocardial damage. This study shows the existence of topographic differences in the tolerance to ischemia in the mid area, subendocardium, and subepicardium; that the sequestration of Ca2+ by mitochondria is an energy-requiring (active) process that occurs only during reperfusion; the loss of the sarcolemma's ability to bind Ca2+ during ischemia to coincide with increased Ca2+ entry during postischemic reperfusion (this Ca2+ is scavenged by mitochondria as long as sufficient energy remains available; these changes are interpreted as being at the edge of irreversibility); and the lack of additional damage and and lack of Ca2+ accumulation in mitochondria during reperfusion in cells that are damaged to such an extent that mitochondria possess flocculent densities already at the end of the ischemic insult.


This article has been cited by other articles:


Home page
J. Pharmacol. Exp. Ther.Home page
D. A. Liem, C. C. Gho, B. C. Gho, S. Kazim, O. C. Manintveld, P. D. Verdouw, and D. J. Duncker
The Tyrosine Phosphatase Inhibitor Bis(Maltolato)Oxovanadium Attenuates Myocardial Reperfusion Injury by Opening ATP-Sensitive Potassium Channels
J. Pharmacol. Exp. Ther., June 1, 2004; 309(3): 1256 - 1262.
[Abstract] [Full Text] [PDF]


Home page
Cardiovasc ResHome page
B. J.J.M Brundel, J. Ausma, I. C van Gelder, J. J.L Van Der Want, W. H van Gilst, H. J.G.M Crijns, and R. H Henning
Activation of proteolysis by calpains and structural changes in human paroxysmal and persistent atrial fibrillation
Cardiovasc Res, May 1, 2002; 54(2): 380 - 389.
[Abstract] [Full Text] [PDF]


Home page
Cardiovasc ResHome page
P. D Verdouw, M. A van den Doel, S. de Zeeuw, and D. J Duncker
Animal models in the study of myocardial ischaemia and ischaemic syndromes
Cardiovasc Res, July 1, 1998; 39(1): 121 - 135.
[Full Text] [PDF]


Home page
Cardiovasc ResHome page
D. J Duncker, R. Schulz, R. Ferrari, D. Garcia-Dorado, C. Guarnieri, G. Heusch, and P. D Verdouw
"Myocardial stunning": remaining questions
Cardiovasc Res, June 1, 1998; 38(3): 549 - 558.
[Full Text] [PDF]




HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Copyright © 1987 by the American Society for Investigative Pathology.