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Articles in PresS, published online ahead of print May 2, 2002
Am J Physiol Heart Circ Physiol, 10.1152/ajpheart.00065.2002
Submitted on January 24, 2002
Accepted on April 26, 2002
1 Department of Cardiology, Hospital Universitari Vall d'Hebron, Barcelona, Spain
2 Department of Cellular Biology and Pathology, Hospital Clinic, Barcelona, Spain
* To whom correspondence should be addressed. E-mail: dgdorado{at}hg.vhebron.es.
Platelets accumulate in reperfused myocardium but their effect on myocardial necrosis has not been established. We tested the hypothesis that the effect of platelets depends on their activation status. Pig platelets were obtained either before a 48-min coronary occlusion (PreCO-plt), 10 min after reperfusion (R-plt), or after 60 min of sham operation (Sham-plt), and were infused into isolated rat hearts (n=124) subsequently submitted to 60 min of ischemia and 60 min of reperfusion. P-selectin expression was higher (p=0.02) in R-plt than in PreCO-plt or Sham-plt. Lactate dehydrogenase (LDH) release during reperfusion was similar in hearts receiving PreCO-plt, Sham-plt or no platelets, but R-plt increased LDH release by 60% (p=0.004). Activation of PreCO-plt with thrombin increased P-selectin expression and LDH release (p<0.001), and these results were unaffected by tirofiban. There was a close correlation between P-selectin expression and LDH release (r=0.84;p<0.001), and myocardial platelet accumulation (r=0.85;p<0.001). We conclude that the deleterious effect of platelets on reperfused myocardium depends on their activation status as represented by P-selectin expression, which is enhanced by ischemia-reperfusion.
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