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Objective: It was known that neutrophils play an important role in ischemic-reperfusion injury. In this study we tested the effect and its mechanism of dipyridamole on neutrophils. Methods:Hydrogen peroxide(H2O2) production by neutrophils was determined using luminol amplified chemiluminescence and the percentage of activity was calculated by observing the uninhibited peak height. Results: Dipyridamole per se produced a concentration-dependent inhibition of H2O2 by formyl-MetleuPhe(fMLP)-stimulated neutrophils. Dipy-ridamole at a low concentration(0.3μmol·L-1) that per se affected neutrophils only slightly, enhanced markedly the effects of adenosine on neutrophils. On the other hand, dipyridamole did not alter the inhibitory effect of NECA(5'-N-ethylcarboxamidoadenosine) on neutrophils. However, propentofylline, a known inhibitor of adenosine uptake, also gotten the same result. Conclusion:Dipy-ridamole inhibited the production of H2O2 by fMLP-stimulated neutrophils. Dipyridamole at a low concentration enhanced the inhibi-tory effect of adenosine on neutrophils. The mechanism involved is probably due to the effect of dipyridamole on adenosine uptake.
Objective: It was known that neutrophils play an important role in ischemic-reperfusion injury. In this study we tested the effect and its mechanism of dipyridamole on neutrophils. Methods: Hydrogen peroxide (H2O2) production by neutrophils was determined using luminol amplified chemiluminescence and the percentage of activity was calculated by observing the uninhibited peak height. Results: Dipyridamole per se produced a concentration-dependent inhibition of H2O2 by formyl-MetleuPhe (fMLP) -stimulated neutrophils. Dipyridamole at a low concentration (0.3 μmol·L-1 ) that per se affected neutrophils only slightly, enhanced markedly the effects of adenosine on neutrophils. On the other hand, dipyridamole did not alter the inhibitory effect of NECA (5'-N-ethylcarboxamidoadenosine) on neutrophils. However, propentofylline, a known inhibitor of adenosine uptake, also gotten the same result. Conclusion: Dipy-ridamole inhibited the production of H2O2 by fMLP-stimulated neutrophils. Dipyridamole at a low concentration enhanced the inhibi-tory effect of adenosine on neutrophils. The mechanism involved probably is due to the effect of dipyridamole on adenosine uptake.