AIM: To investigate the effects of different concentrations of thrombin, arachidonic acid (AA) and aspirin on leukocyte-platelet adhesion. METHODS: The methods of Hamburger et al and Shen Zhi-qiang et al were used to study the adhesion between platelets and leukocytes in rats. RESULTS: 50 U/L of thrombin markedly stimulated the binding between platelets and leukocytes; the efficacy of thrombin increased with its concentration and produced the maximum effect at 300 U/L. But the adhesion rate decreased while the concentration of thrombin was more than 300 U/L. 25 ?mol/L of AA significantly enhanced the binding of platelets to leukocytes; the efficacy of AA increased with its concentration and obtained the maximum effect at 100 ?mol/L. The adhesion rate, however, decreased while the concentration of AA was more than 100 ?mol/L. Aspirin could inhibit thrombin-or AA-induced adhesion between platelets and leukocytes. CONCLUSION: It is suggested that thrombin and AA, in a certain range of concentrations, concentration-dependently induced the binding of platelets to leukocytes; the adhesive rate, however, decreased as the concentration of the above inducers increased. Aspirin could inhibit platelet-leukocyte adhesion stimulated by thrombin and AA.

AIM: To investigate the effect of non-activated or activated polymorphonuclear leukocytes(PMN) on washed platelet aggregation. METHODS: Born's method was used to determine platelet aggregation.RESULTS: non-activated PMN (5?10 9 cells/L) significantly suppressed washed platelet aggregation induced by ADP or arachidonic acid. Aspirin enhanced this inhibition. N-formyl-methiongl-leucy-phenylalanine (fMLP)-or platelet-activating factor (PAF)-stimulated PMN strongly induced platelet aggregation, and the induction effect of PMN suspension was more active than that of PMN supernatant. Aspirin had no significant inhibitory effect on platelet aggregation induced by fMLP-or PAF-activated PMN. CONCLUSIONS: Different conditions of PMN (activated or non-activated) had the nearly opposite action on normal platelet reactivity. Briefly, non-activated-PMN inhibited platelet reactivity, whereas activated PMN stimulated it.