Brain death does not change epicardial action potentials and their response to ischemia-reperfusion in open-chest
Georges Christé1, Guylaine Hadour, Michel Ovize
1INSERM EMI-0219, Laboratoire de Développement et Vieillissement de l'Endothélium, CEA Grenoble, Grenoble. christe@lyon.inserm.fr
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 (APD50) had a linear relationship to the cardiac inter-beat (RR) interval (R2 = 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.
