JTCS St. Jude Medical
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 HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Kao, R. L.
Right arrow Articles by Magovern, G. J.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Kao, R. L.
Right arrow Articles by Magovern, G. J.

The Journal of Thoracic and Cardiovascular Surgery, Vol 91, 106-114, Copyright © 1986 by The American Association for Thoracic Surgery and The Western Thoracic Surgical Association

ARTICLES

Prevention of reperfusional damage from ischemic myocardium

RL Kao and GJ Magovern

Reperfusional damage refers to the serious structural, functional, and metabolic derangements commonly observed during restoration of coronary circulation following cardiopulmonary bypass. Damage is believed to result from ischemic injury incurred during aortic cross-clamping and unmasked in the recovery period and/or certain metabolic processes activated during postischemic reperfusion. It has been postulated that reperfusional damage can be minimized or eliminated if normal myocardial metabolic parameters can be maintained or restored before the initiation of reperfusion. Studies have tested a variety of cardioplegic solution compositions and administration modes. However, much controversy exists over the different methods. We have tested the hypothesis that improved myocardial protection during cardioplegia can prevent reperfusional damage and investigated the possibility of achieving optimal myocardial protection. Elective cardiac arrest was induced in isolated perfused rat hearts, under working conditions reported previously. We tested two arresting temperatures (8 degrees C and 28 degrees C), three infusion frequencies (single, double, and multiple dose), and different combinations of cardioplegic additives with demonstrated benefits (glucose, adenosine, creatine, and albumin). Metabolic and hemodynamic functions were used to evaluate the protection of the ischemic myocardium. Glucose (0.5%) and adenosine (1 mmol/L) provided clear benefits under all experimental conditions. Double-dose cardioplegia at 8 degrees C also surpassed the single- and multiple-dose groups. When oxygenated cardioplegic solution containing glucose and adenosine was reinfused for 1 minute after 30 minutes of cross-clamping, no measurable changes were detected after ischemic arrest, as compared with normal hearts. Reperfusional damage was eliminated by this procedure. We concluded that an optimal condition for myocardial preservation during elective cardiac arrest in our model was established.


This article has been cited by other articles:


Home page
 Ann. Thorac. Surg.Home page
X.-H. Ning, Keith.F. Childs, and S. F. Bolling
Glucose Level and Myocardial Recovery After Warm Arrest
Ann. Thorac. Surg., December 1, 1996; 62(6): 1825 - 1829.
[Abstract] [Full Text]


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 © 1986 by The American Association for Thoracic Surgery.