Brain death further promotes ischemic reperfusion injury of the rabbit myocardium

Background. Little is known about preload-dependent cardiac function after brain death (ED) and subsequent graft preservation. Methods. A validated model of ED in rabbits was developed and myocardial performance was studied after ED induction and I 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 ED. After global hypothermic ischemia, significant decreases in stroke work, left ventricular contractility, and left ventricular relaxation were observed in the ED group compared with controls. Cardiac output and coronary flow were also significantly decreased in ED hearts compared with controls. Creatine kinase release was increased by 32.5% in BD hearts compared with controls. Conclusions. In a rabbit model, ED 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 ED hearts.