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Shankha S. Biswas
Edward P. Chen
Hartmuth B. Bittner
Peter Van Trigt, III
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Ann Thorac Surg 1996;62:1808-1815
© 1996 The Society of Thoracic Surgeons

Original Articles: Cardiovascular

Brain Death Further Promotes Ischemic Reperfusion Injury of the Rabbit Myocardium

Shankha S. Biswas, MD, Edward P. Chen, MD, Hartmuth B. Bittner, MD, PhD, R. Duane Davis, MD, Peter Van Trigt, III, MD

Division of Cardiovascular and Thoracic Surgery, Department of Surgery, Duke University Medical Center, Durham, North Carolina

Accepted for publication July 2, 1996.

Background. Little is known about preload-dependent cardiac function after brain death (BD) and subsequent graft preservation.

Methods. A validated model of BD in rabbits was developed and myocardial performance was studied after BD induction and 1 hour of subsequent global hypothermic ischemia using a validated rabbit model and an isolated work-performing heart preparation.

Results. Significant decreases in stroke work, left ventricular contractility, and left ventricular relaxation were observed 2 hours after BD. After global hypothermic ischemia, significant decreases in stroke work, left ventricular contractility, and left ventricular relaxation were observed in the BD group compared with controls. Cardiac output and coronary flow were also significantly decreased in BD hearts compared with controls. Creatine kinase release was increased by 32.5% in BD hearts compared with controls.

Conclusions. In a rabbit model, BD combined with global hypothermic ischemia causes a significant decrease in left ventricular function compared with global hypothermic ischemia. This dysfunction may be attributed to a significant decrease in coronary flows in BD hearts.




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