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

被引:8
作者
Lee, JR
Han, JJ
Seo, JW
机构
[1] Seoul Natl Univ, Med Res Ctr, Seoul, South Korea
[2] Seoul Natl Univ, Coll Med, Seoul Natl Univ Hosp, Dept Thorac & Cardiovasc Surg & Pathol, Seoul, South Korea
[3] Ewha Womans Univ, Coll Med, Ewha Univ Mokdong Hosp, Dept Thorac & Cardiovasc Surg, Seoul, South Korea
关键词
D O I
10.1016/S0003-4975(00)01938-X
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
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 degreesC 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. (Ann Thorac Surg 2000;70:1531-5) (C) 2000 by The Society of Thoracic Surgeons.
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页码:1531 / 1535
页数:5
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