ATS
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
 QUICK SEARCH:   [advanced]


     


This Article
Right arrow Full Text
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Email this article to a friend
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 Add to Personal Folders
Right arrow Download to citation manager
Right arrow Permission Requests
Citing Articles
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Barbé, C. C.
Right arrow Articles by Bonnet, P. M.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Barbé, C. C.
Right arrow Articles by Bonnet, P. M.

Ann Thorac Surg 1997;63:1303-1308
© 1997 The Society of Thoracic Surgeons


Original Article: Cardiovascular

Cardioplegia Preserves Hypoxic Response in Isolated Coronary Arteries but Not in Isolated Hearts

Christine C. Barbé, MS, Frank F. Diemont, MD, Pierre M. Bonnet, MD, PhD

UMR Centre National de la Recherche Scientifique 6542, Physiologie des Cellules Cardiaques et Vasculaires, Faculté des Sciences, Tours, France

Accepted for publication November 19, 1996.

Background. Experiments were designed to determine whether hyperkalemic crystalloid cardioplegic solution alters the hypoxic response of isolated segments of rabbit coronary arteries.

Methods. Coronary arteries were suspended in organ chambers to measure isometric force. We measured the coronary perfusion pressure at a constant flow rate in isolated Langendorff-perfused hearts. Coronary arteries and hearts were preserved in warm (37°C) physiologic solution or in cold (10°C) crystalloid cardioplegic solution.

Results. In all groups of coronary arteries, the acetylcholine-induced relaxation before and after preservation was unchanged (n = 7). Hypoxia (15 mm Hg) caused an endothelium-dependent contraction, the amplitude of which did not change after cardioplegia. Conversely, in coronary arteries preserved in physiologic solution, hypoxic contraction amplitude decreased by 67% ± 17%. In isolated hearts, hypoxic perfusion (15 mm Hg) induced a vasodilation. In all groups, the second hypoxic vasodilation was significantly greater (group 1, first hypoxic perfusion 2.8% ± 2.8%, second hypoxic perfusion 18.2% ± 7.1%; group 2, first hypoxic perfusion 6.8% ± 1.5%, second hypoxic perfusion 29% ± 9%).

Conclusions. The crystalloid cardioplegic solution did not change the hypoxic response in isolated hearts and preserved the endothelium-dependent hypoxic contraction in coronary arteries.







HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
ANN THORAC SURG ASIAN CARDIOVASC THORAC ANN EUR J CARDIOTHORAC SURG
J THORAC CARDIOVASC SURG ICVTS ALL CTSNet JOURNALS
Copyright © 1997 by The Society of Thoracic Surgeons.