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Ann Thorac Surg 1995;60:1729-1734
© 1995 The Society of Thoracic Surgeons

Original Articles: Cardiovascular

Myocardial Effects of Experimental Acute Brain Death: Evaluation by Hemodynamic and Biological Studies

Georges Pinelli, MD, Paul-Michel Mertes, MD, PhD, Jean-Pierre Carteaux, MD, Yves Jaboin, Jean-Marie Escanye, PhD, François Brunotte, MD, Jean-Pierre Villemot, MD

Service de Chirurgie Cardiaque et Transplantations Cardio-thoraciques, Centre Hospitalo-Universitaire de Nancy-Brabois, and Laboratoires de Chirurgie Expérimentale and de Biophysique, Faculté de Médecine de Nancy, Vandoeuvre les Nancy, France

Accepted for publication July 29, 1995.

Background. Because of problems concerning the functional quality of heart transplants, more and more interest has been focused on the physiologic changes occurring during brain death, one of the major possible contributing factors to the myocardial alterations.

Methods. The aim of this study was to describe the link between acute experimental brain death and myocardial metabolism. This was achieved by in vivo 3-hour hemodynamic and biological (myocardial lactate production) studies and then in vitro 6-hour phosphorus-31 nuclear magnetic resonance spectroscopy. Two groups of pigs were involved in the study: group I (n = 10) as control and group II (n = 10) as brain-dead animals.

Results. Within the first hour, we observed a strong increase in myocardial activity associated with the onset of myocardial lactate production, lasting 2 hours and corresponding to a myocardial anaerobic metabolism period. Despite the apparent normalization before excision of the hearts, phosphorus-31 nuclear magnetic resonance spectroscopy revealed a significant decrease in adenosine triphosphate levels in group II when compared with group I.

Conclusions. We conclude that, in our study, acute experimental brain death is associated with an early and transient period of myocardial anaerobic metabolism and adenosine triphosphate consumption. These myocardial consequences of brain death could partially explain some observations of heart graft dysfunction.






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Copyright © 1995 by The Society of Thoracic Surgeons.