Correlation between ICAM-1 and functional recovery of piglet myocardium with leukocyte-depleted reperfusion.

Abstract

Reperfusion injury involves leukocyte-endothelial interaction mediated by cell adhesion molecules. This study was designed to determine the time course of intercellular adhesion molecule-1 (ICAM-1) expression and the functional recovery of myocardium when reperfused with leukocyte depleted whole blood. Sixteen neonatal piglet hearts were harvested and stored with 4 degrees C cold University of Wisconsin Solution (UWS) for 12 hours. An ex vivo model consisting of an isolated working heart perfusion circuit, roller pumps, and a membrane oxygenator, was used for reperfusion. Atrial tissues were taken for staining ICAM-1. The stroke work index (SWI) was calculated during 4 hours of reperfusion. Two groups (group 1: reperfused with whole blood, group 2: with leukocyte depleted blood) were compared. The differences of ICAM-1 expression between group 1 and 2 were significant at 3 and 4 hours of reperfusion (p < 0.05). The differences of the mean stroke work indices were significant at 2, 3, and 4 hours after reperfusion (p < 0.05). Leukocyte-depleted reperfusion attenuates the expression of ICAM-1 and reduces the time-dependent functional deterioration of the myocardium. These results suggest that adhesion molecule like ICAM-1 plays a major role in deteriorating myocardial function during the reperfusion, possibly by leukocyte-mediated inflammatory process.