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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
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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