BRAIN-DEATH FURTHER PROMOTES ISCHEMIC REPERFUSION INJURY OF THE RABBIT MYOCARDIUM

Background. Little is known about preload-dependent cardiac function a fter brain death (ED) and subsequent graft preservation. Methods. A va lidated model of ED in rabbits was developed and myocardial performanc e was studied after ED induction and I hour of subsequent global hypot hermic ischemia using a validated rabbit model and an isolated work-pe rforming heart preparation. Results. Significant decreases in stroke w ork, left ventricular contractility, and left ventricular relaxation w ere observed 2 hours after ED. After global hypothermic ischemia, sign ificant decreases in stroke work, left ventricular contractility, and left ventricular relaxation were observed in the ED group compared wit h controls. Cardiac output and coronary flow were also significantly d ecreased in ED hearts compared with controls. Creatine kinase release was increased by 32.5% in BD hearts compared with controls. Conclusion s. In a rabbit model, ED combined with global hypothermic ischemia cau ses a significant decrease in left ventricular function compared with global hypothermic ischemia. This dysfunction may be attributed to a s ignificant decrease in coronary flows in ED hearts.