Clot Promoting Effect of Platelet-Vessel wall Interaction

When a piece of vascular tissue (rat, rabbit) is incubated in plasma, clotting occurs. The presence of platelets accelle rates this clotting process. Inhibition of vascular prostacyclin (PGI₂) production, either by drugs or by inducing arachidonic acid deficiency, causes the platelets to become activated by the vessel wall, resulting in platelet shape change and -aggregation and in a further enhancement of the coagulation response. Hirudin very actively inhibits both aggregation and clotting whereas ADP scavenging has only a weak effect. This indicates that the aggregation response, occurring upon plateletvessel wall interaction is for the greater part mediated by thrombin. Saturated fat feeding increases the clot promoting effect of the platelet-vessel wall interaction. This appeared not to be due to differences in the production of vascular PGI₂ or platelet endoperoxides and thromboxanes (measured as malondialdehyde). These findings indicate that:

1. Thrombin, locally generated upon the interaction between damaged vessel wall and blood constituents, contribute to arte rial thrombus formation;

2. Prostacyclin regulates local thrombin formation viaits inhibiting effect on platelet activation;

3. The existence of another, platelet bound affector is postulated.