Key result
ICAM-1 and P-selectin deficiency reduces neutrophil influx but fails to reduce myocardial infarct size.
P-selectin and intercellular adhesion molecule-1 (ICAM-1) mediate early interaction and adhesion of neutrophils to coronary endothelial cells and myocytes after myocardial ischemia and reperfusion. In the present study, we examined the physiological consequences of genetic deletions of ICAM-1 and P-selectin in mice. In wild-type mice, after 1 h of ischemia followed by reperfusion, neutrophil influx into the area of ischemia was increased by 3 h with a peak at 24 h and a decline by 72 h. ICAM-1/P-selectin-deficient mice showed a significant reduction in neutrophils by immunohistochemistry or by myeloperoxidase activity at 24 h but no significant difference at 3 h. Infarct size (area of necrosis/area at risk) assessed 24 h after reperfusion was not different between wild-type and deficient mice after 30 min and 1 h of occlusion. Mice with a deficiency in both ICAM-1 and P-selectin have impaired neutrophil trafficking without a difference in infarct size due to myocardial ischemia-reperfusion.
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Briaud et al. (2001) studied Myocardial ischemia and reperfusion injury. Genetic deletion of ICAM-1 and P-selectin vs. Wild-type mice was evaluated on Neutrophil influx and infarct size (area of necrosis/area at risk) at 24 h after reperfusion. ICAM-1/P-selectin deficiency in mice significantly reduced neutrophil influx at 24 h post-reperfusion without altering myocardial infarct size after 30 min or 1 h of coronary occlusion.
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