Brain Death Does Not Change Epicardial Action Potentials and Their Response to Ischemia–Reperfusion in Open-chest Pigs

Background It is debated whether brain death (BD) causes transient functional ischemia. In this investigation we used monophasic action potential (AP) recording during BD as a sensitive means to assess: (i) whether ischemia was present; and (ii) the effect of BD on a subsequent ischemia–reperfusion challenge. Methods In Period 1, BD was induced (BD group, 6 pigs) or not induced (sham maneuver, control [C] group, 6 pigs), and effects were followed for 3 hours. In Period 2, left anterior descending (LAD) coronary artery ligation ischemia was applied for 20 minutes to all hearts, followed by 60-minute reperfusion. Results In Period 1, plasma norepinephrine was 3.1-, 6.3- and 5-fold greater in BD than in C at 1, 120 and 180 minutes, respectively, and systolic blood pressure was 26% greater at 1 minute and 35% at 120 minutes. The arteriovenous difference in lactate was similar or lower in BD than in C. In both groups, at all time-points, the action potential recording had a rectangular plateau shape and action potential duration (APD 50 ) had a linear relationship to the cardiac inter-beat (RR) interval ( R 2 = 0.89 and 0.73, slope=0.42 ± 0.02 and 0.46 ± 0.06 in BD and C, respectively). In Period 2, ischemia caused a similar (50%) APD shortening in BD and C. Restoration of the APD upon reperfusion was complete in both groups. Conclusions Our findings suggest that BD does not cause direct cardiac ischemia and does not change the response of the heart to subsequent ischemia–reperfusion challenge.