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Updated: Sep 17, 2026
A Murine Closed-chest Model of Myocardial Ischemia and Reperfusion
Published on: July 17, 2012
Correlation between ICAM-1 and functional recovery of piglet myocardium with leukocyte-depleted reperfusion
1Department of Thoracic and Cardiovascular Surgery, and Pathology, Seoul National University Hospital, Seoul National University College of Medicine, Seoul National University Medical Research Center, Heart Research Institute, Korea. jrl@plaza.snu.ac.kr
Background:
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.
Methods:
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.
Results:
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).
Conclusions:
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.
