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Am J Physiol Heart Circ Physiol 275: H1865-H1872, 1998;
0363-6135/98 $5.00
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Vol. 275, Issue 5, H1865-H1872, November 1998

Coronary endothelial P-selectin in pathogenesis of myocardial ischemia-reperfusion injury

Anthony J. Palazzo1, Steven P. Jones1, Donald C. Anderson2, D. Neil Granger1, and David J. Lefer1

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

We investigated in vivo coronary P-selectin expression and its pathophysiological consequences in a murine model of myocardial ischemia-reperfusion (MI/R) using wild-type and P-selectin deficient (-/-) mice. Coronary P-selectin expression [µg monoclonal antibody (MAb)/g tissue] was measured using a radiolabeled MAb method after 30 min of myocardial ischemia and 20 min of reperfusion. P-selectin expression in wild-type mice was significantly (P < 0.01) elevated in the ischemic zone (0.070 ± 0.010) compared with the nonischemic zone (0.037 ± 0.008). Myocardial P-selectin expression was nearly undetectable in P-selectin -/- mice after MI/R. Furthermore, myocardial infarct size (% of area at risk) after 30 min of myocardial ischemia and 120 min of reperfusion was 42.5 ± 4.4 in wild-type mice and 24.4 ± 4.0 in P-selectin -/- mice (P < 0.05). In additional experiments of prolonged myocardial ischemia (60 min) and reperfusion (120 min), myocardial infarct size was similar in P-selectin -/- mice and wild-type mice. Our results clearly demonstrate the involvement of coronary P-selectin in the development of myocardial infarction after MI/R.

neutrophil; adhesion molecules; infarction; mouse; monoclonal antibody


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