Coronary endothelial P-selectin in pathogenesis of myocardial ischemia-reperfusion injury.
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 [microgram 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.
Palazzo
A J
AJ
Department of Molecular and Cellular Physiology, Louisiana State University Medical Center, Shreveport, Louisiana 71130-3392, USA.
Jones
S P
SP
Anderson
D C
DC
Granger
D N
DN
Lefer
D J
DJ
D000818:Animals; D003331:Coronary Vessels / Q000503:physiopathology*; D004730:Endothelium, Vascular / Q000503:physiopathology*; D051379:Mice; D008822:Mice, Transgenic; D015428:Myocardial Reperfusion Injury / Q000503:physiopathology*; D019007:P-Selectin / Q000502:physiology*
D019007:P-Selectin