HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Add to Personal Folders Download to citation manager Permission Requests Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Jimenez, E. Articles by Levitsky, S. Search for Related Content PubMed PubMed Citation Articles by Jimenez, E. Articles by Levitsky, S.

The Journal of Thoracic and Cardiovascular Surgery, Vol 105, 988-994, Copyright © 1993 by The American Association for Thoracic Surgery and The Western Thoracic Surgical Association

ARTICLES

Redistribution of myocardial calcium during ischemia. Relationship to onset of contracture

E Jimenez, P del Nido, H Feinberg and S Levitsky
Department of Surgery, New England Deaconess Hospital, Boston, Mass.

Cytosolic calcium accumulation has been proposed as a mediator for the pathologic changes that occur during myocardial ischemia. Whether the rise in cytosolic calcium is a result of influx or redistribution from internal stores has not been elucidated. Isolated retroperfused rabbit hearts were subjected to ischemia at 37 degrees C. The distribution of calcium between cytosol and internal membrane stores and the relationship between cytosolic calcium and the onset of left ventricular contracture were investigated. One group of hearts was loaded with the fluorescent calcium probe Fura 2-AM to measure cytosolic calcium and a second group with chlortetracycline to indicate changes in membrane-bound calcium. After the onset of ischemia there is a rise in cytosolic calcium, at least in part attributable to redistribution of calcium from intraorganellar sites to cytosol. The release of membrane-bound calcium and rise in cytosolic calcium preceded the onset of irreversible ischemic injury, that is, contracture.

This article has been cited by other articles:

				C. Stamm, I. Friehs, Y.-H. Choi, D. Zurakowski, F. X McGowan, and P. J del Nido Cytosolic calcium in the ischemic rabbit heart: assessment by pH- and temperature-adjusted rhod-2 spectrofluorometry Cardiovasc Res, September 1, 2003; 59(3): 695 - 704. [Abstract] [Full Text] [PDF]

				M. Munakata, C. Stamm, I. Friehs, D. Zurakowski, D. B. Cowan, H. Cao-Danh, F. X. McGowan Jr, and P. J. del Nido Protective effects of protein kinase C during myocardial ischemia require activation of phosphatidyl-inositol specific phospholipase C Ann. Thorac. Surg., April 1, 2002; 73(4): 1236 - 1245. [Abstract] [Full Text] [PDF]

				K. Takeuchi, P. Buenaventura, H. Cao-Danh, P. Glynn, E. Simplaceanu, F. X. McGowan, and P. J. del Nido Improved Protection of the Hypertrophied Left Ventricle by Histidine-Containing Cardioplegia Circulation, November 1, 1995; 92(9): 395 - 399. [Abstract] [Full Text]

				A. Ohkado, H. Cao-Danh, K. E. Sommers, and P. J. del Nido Evaluation of highly buffered low-calcium solution for long-term preservation of the heartComparison with University of Wisconsin solution J. Thorac. Cardiovasc. Surg., October 1, 1994; 108(4): 762 - 771. [Abstract] [Full Text]