Brain Death Does Not Change Epicardial Action Potentials and Their Response to Ischemia–Reperfusion in Open-chest Pigs
Résumé
Background: It is debated whether brain death (BD) causes transient functional ischemia. Here we used monophasic action potential (AP) recording, as a sensitive means to assess, during BD, (i) whether ischemia was present, (ii) the effect of BD on a subsequent ischemia-reperfusion challenge. Methods: Period 1: BD was induced (BD group, six pigs) or not (sham maneuver, C group, six pigs) and effects were followed up for 3 hours. Period 2: LAD ligation ischemia was applied for 20 min to all hearts, and was followed by 60-min reperfusion. Results: Period 1: plasma norepinephrine was 3.1, 6.3 and 5 fold larger in BD versus C at respectively 1, 120 and 180 minutes and systolic blood pressure was larger by 26% at 1 min and 35% at 120 minutes. The arterio-venous difference in lactate was similar or lower in BD versus C. In both groups, at all times, AP had rectangular plateau shape and the action potential duration (APD 50) followed a linear relationship to the RR interval (R 2 = 0.89 and 0.73, slope = 0.42±0.02 and 0.46±0.06 in BD and C respectively). Period 2: ischemia caused a similar (50%) APD shortening in BD and C. Restoration of APD upon reperfusion was complete in both groups. Conclusions: These data suggest that BD does not cause direct cardiac ischemia and does not change the response of the heart to subsequent ischemia-reperfusion challenge.
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