|
|
||||||||
| ||||||||||||||||||||||||||||||||||||||||||||||||||
Ann Thorac Surg 1995;60:1192
© 1995 The Society of Thoracic Surgeons
DR HENDRICK B. BARNER (St. Louis, MO): I understand that Dr Weschler's group showed that it took a greater ischemic insult to produce endothelial injury. You did not tell us what your myocardial temperature was and how frequently cardioplegia was reinfused. What the clinician wants to know is whether 2 hours of cardioplegic arrest would achieve endothelial injury, or does it take a greater ischemic insult to achieve endothelial injury?
DR HIRAMATSU: We usually cooled the myocardial temperature to 15°C, and during the 2 hours of cardiac arrest, myocardial temperature was just under 15°C. I think it is cool enough.
DR BARNER: How frequently is cardioplegia given?
DR HIRAMATSU: We give a 20 mL/kg initial dose of cardioplegia and after 1 hour of cardiac arrest I add 10 mL/kg of cardioplegia.
DR JOHN W. HAMMON, JR (Winston-Salem, NC): That was very nicely done. In isolated blood-perfused heart preparations, it is difficult to know if neutrophils are present in the perfusate. Given that the mechanism of endothelial injury probably involves neutrophils, did you assay your preparation for neutrophils?
DR HIRAMATSU: Most recently we did another set of experiments on l-arginine. We measured the myeloperoxidase activity, and l-argininetreated hearts had significantly reduced activity of myeloperoxidase. We think that inhibition of neutrophil adhesion is a major beneficial effect of l-arginine.
Related Article
Ann. Thorac. Surg. 1995 60: 1187-1192.
| ||||||||||||||||||||||||||||||||||||||||||||||||||
| 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 |