We have discovered that bcrberine (BR) is an anti-platelet drug.It was demonstrated that BR inhibited ADP-, arachidonate-, collagen-and calcium ionophorc A231S7-xnduced platelet aggregation and ATP release in different degrees.Especially BR strongly inhibited collagen-induced platelet aggregation and ATP release reaction(IC50 values were 0.12 and 0.08 mmol/L,respectively).The antiplatekt mechanism of BR may be inhibition of arachidonate metabolism,, and suppression of the rise of intracdlular Ca2' and/or cAMP levels.Because the platelet thrombus foimation in the arteries of brain and heart is closely related to the subendothelial collagen fibrils, BR may be an effective drug for the patients with these diseases.

Al8+ is a newly discovered antiplatelet agent. It was demonstrated that Al3+ inhibited platelet aggregation induced by ADP, arach.idona.te or collagen and also had a deaggregatory effect on platelet aggregates induced by ADP or arachidonate. Both effects were related to the concentration ratio of Ca2+ to Al3+ added.Therefore, it suggests that the antiplatelet effects of Al3+ may be competitive with Ca2+ to the calcium-dependent events in/on platelets. However, the platelet aggregates induced by collagen are not deaggregated by Al3+.So, all the results can clinically be used to explain the gastro-intestinal hemorrhage in the aluminum toxicity and theoretically support the classification of the interplatelet bridges into two kinds: the reversible and irreversible.

An investigation of the correlation between platelet activity and extracellular Ca2+concentration is described.It was demonstrated that in the citrate-platelet-rich-plasma of rabbits and rats,the rate of shape change of the platelets induced by different activators did not alter when different doses of calcium ions were added to the experimental system, while the platelet activity of both secretion and aggregation was increased along with increased doses of calcium ions. Therefore, in the animal experiment addition of an appropriate dose of calcium ions to the citrate-platelet-rich-plasma is necessary to allow full play to the functional activity of platelets, and to maintain calcium-dependent reaction.

After the antiaggregatory effect of pilocarpine on platelets was discovered, we continued to demonstrate its other effects on platelets. The results of the experiments with rabbit platelets were as follows. (1)Pilocarpine inhibited platelet aggregation and ATP secretion induced by ADP, arachidonate and collagen; it inhibited platelet shape change induced by collagen, but not by ADP and arachidonate. (2)Pilocarpine deaggregated the platelet aggregates induced by ADP and arachidonate, but had no such effect on those induced by collagen. The interplatelet bridge demonstrated by Nachman et al can not reasonably explain the latter phenomenon, we suggest two hypothetical models of interplatelet bridge with glycoprotein G(GPG)as a component.

We found that the platelet aggregation rates induced by ADP, arachidonic acid (AA), collagen and A23187 had an apparent decreasing after injection of berberine into the vein of rabbits, and also found that berberine had an apparent inhibition of calcium influx into platelet induced by A23187 at lower concentrations. We demonstrated that berberine had no obvious effect on cAMP level in the intact platelet of rabbits.