The expression of the CD18 leucocyte integrin in a rabbit model of acute myocardial infarction: A pilot study of temporal changes and relationship toinfarct size

Citation
G. Hillis et al., The expression of the CD18 leucocyte integrin in a rabbit model of acute myocardial infarction: A pilot study of temporal changes and relationship toinfarct size, CARDIOLOGY, 95(1), 2001, pp. 35-39
Citations number
22
Categorie Soggetti
Cardiovascular & Respiratory Systems","Cardiovascular & Hematology Research
Journal title
CARDIOLOGY
ISSN journal
00086312 → ACNP
Volume
95
Issue
1
Year of publication
2001
Pages
35 - 39
Database
ISI
SICI code
0008-6312(2001)95:1<35:TEOTCL>2.0.ZU;2-O
Abstract
CD18 integrins mediate leucocyte adhesion to vascular endothelium. This rep resents the initial step in inflammatory cell infiltration following myocar dial necrosis. The current study assessed whether the expression of these r apidly activated and readily measured adhesion receptors on circulating neu trophils would reflect the extent of cardiac damage in a rabbit model of ac ute myocardial infarction. Myocardial ischaemia/infarction was induced in a naesthetised adult male New Zealand white rabbits (n = 8) by ligation of th e circumflex or marginal coronary artery. To control for the effects of ana esthesia and surgery, 4 rabbits underwent identical procedures without the induction of infarction. Absolute infarct size (in mg) and infarct size as a percentage of total left ventricular mass (relative infarct size) were ca lculated by differential staining and weighing of necrotic myocardium. Flow cytometry was used to determine cell surface expression of CD18 at six tim e points (baseline, 20 and min of ischaemia and 20, 60 and 180 min of reper fusion). Absolute neutrophil CD18 expression and changes in expression over baseline were correlated with absolute and relative infarct size. Mean neu trophil CD18 expression increased significantly (from 2.42 +/- 0.20 to 3.07 +/- 0.29; p = 0.04) within 20 min of ischaemia. CD18 expression at 3 h did not predict absolute or relative infarct size (r = 0.40 and 0.37, respecti vely). The percent age change in cell surface CD18 expression (above baseli ne levels) was, however, correlated with both measures of infarct size (r = 0.76, p = 0.03, and r = 0.92, p = 0.001, respectively). In conclusion, in this rabbit model of myocardial infarction, neutrophil CD18 expression rise s within 20 min of the induction of ischaemia but absolute values after 3 h of reperfusion are poor indicators of infarct size. Although percentage ch ange in neutrophil CD18 levels over baseline correlates with infarct size t here is considerable variation between individuals, limiting any clinical a pplication. Copyright (C) 2001 S. Karger AG, Basel.