JTCS Click here to go to SJM website.
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
 QUICK SEARCH:   [advanced]


     


This Article
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
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 Ohnuki, M.
Right arrow Articles by Suzuki, A.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Ohnuki, M.
Right arrow Articles by Suzuki, A.

The Journal of Thoracic and Cardiovascular Surgery, Vol 106, 172-179, Copyright © 1993 by The American Association for Thoracic Surgery and The Western Thoracic Surgical Association


ARTICLES

Mechanism of changes of the collagen matrix of reperfused myocardium in donor heart preservation

M Ohnuki, M Sunamori, J Amano and A Suzuki
Department of Thoracic-Cardiovascular Surgery, Tokyo Medical and Dental University, School of Medicine, Japan.

Isolated canine hearts were preserved for 6 hours at 5 degrees C followed by normothermic reperfusion for 2 hours. Dogs were divided into two groups: group I (group Ia [n = 7] and group Ib [n = 3] with the left ventricle unloaded during reperfusion) received a preservation solution containing potassium (20 mmol/L), and group II (n = 9) received University of Wisconsin solution. Left ventricular diastolic function was better preserved in group II. Degradation and loss of the collagen network during reperfusion, as assessed by scanning electron microscopy, were more extensive and significantly more frequent in group Ia than in group II (6/7 versus 2/9; p < 0.05). Furthermore, extensive disruption of the collagen network was significantly more prevalent in hearts with a left ventricular end-diastolic pressure of more than 20 mm Hg than in hearts with a left ventricular end-diastolic pressure of less than 20 mm Hg (8/10 versus 0/6; p < 0.05), and no disruption of the collagen network occurred in group Ib, regardless of the type of preservation solution. These results suggest that the greatest disruption is caused by barotrauma resulting from an elevated left ventricular end-diastolic pressure after ventricular dysfunction caused by ischemic reperfusion injury.





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 © 1993 by The American Association for Thoracic Surgery.