Myocardial ischemia-reperfusion injury in CD18- and ICAM-1-deficient mice

Citation
Aj. Palazzo et al., Myocardial ischemia-reperfusion injury in CD18- and ICAM-1-deficient mice, AM J P-HEAR, 44(6), 1998, pp. H2300-H2307
Citations number
40
Categorie Soggetti
Cardiovascular & Hematology Research
Journal title
AMERICAN JOURNAL OF PHYSIOLOGY-HEART AND CIRCULATORY PHYSIOLOGY
ISSN journal
03636135 → ACNP
Volume
44
Issue
6
Year of publication
1998
Pages
H2300 - H2307
Database
ISI
SICI code
0363-6135(199812)44:6<H2300:MIIICA>2.0.ZU;2-Z
Abstract
Previous studies have demonstrated that circulating neutrophils (PMNs) cont ribute to the pathophysiology of myocardial ischemia-reperfusion (MYR) inju ry. PMN-endothelial cell interactions are highly regulated by adhesive inte ractions between PMN CD11/ CD18 and coronary endothelial cell intercellular adhesion molecule-1 (ICAM-1). We investigated the effects of MI/R in wild- type, CD18-, and ICAM-1-deficient (-/-) mice. Wildtype (n = 6), CD18 -/- (n . = 6), and ICAM-1 -/- (n = 6) mice were subjected to 30 min of myocardial ischemia and 120 min of reperfusion to determine the extent of PMN infiltra tion and myocardial cell necrosis. Myocardial infarction (% of the area at risk) was 45.1 +/- 5.9 in wild-type mouse hearts. In contrast, the extent o f myocardial infarction was significantly (P < 0.05) reduced in the CD18 (1 9.3 +/- 5.1%)- and ICAM-1 (17.9 +/- 3.2%)-deficient mice. Similarly, PMN in filtration into the ischemic-reperfused myocardium was attenuated by 54% in the CD18 -/- mice and by 32% in ICAM-1 -/- mice compared with wild-type he arts. Deficiency in either CD18 or ICAM-1 expression results in a marked re duction in PMN accumulation and myocardial necrosis after acute MI/R.