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1 Department of Molecular and Cellular Physiology, Louisiana State University Medical Center, Shreveport, Louisiana 71130-3392; and 2 Discovery Research, Pharmacia and Upjohn, Kalamazoo, Michigan 49001
Previous studies have demonstrated that
circulating neutrophils (PMNs) contribute to the pathophysiology of
myocardial ischemia-reperfusion (MI/R) injury. PMN-endothelial
cell interactions are highly regulated by adhesive interactions 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. Wild-type
(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 infiltration 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 of myocardial infarction was
significantly (P < 0.05) reduced in
the CD18 (19.3 ± 5.1%)- and ICAM-1 (17.9 ± 3.2%)-deficient mice. Similarly, PMN infiltration into the ischemic-reperfused myocardium was attenuated by 54% in the CD18 / mice and
by 32% in ICAM-1 / mice compared with wild-type hearts.
Deficiency in either CD18 or ICAM-1 expression results in a marked
reduction in PMN accumulation and myocardial necrosis after acute MI/R.
neutrophil; infarction; mouse; intercelleular adhesion molecule-1
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