Plenary Lecture

Abstract

This lecture is concerned mainly with questions about how haemodynamic conditions in atherosclerotic arteries affect arriving platelets that aggregate there and about the chemical agents responsible for making the platelets reactive. The effects of haemodynamic conditions and the agents are known mainly from in vitro experiments in which aggregation can be quantitatively correlated with blood flow and bioch6mical effects by simple and reproducible methods; the relevance to the more complicated situations in haemostasis and thrombosis is uncertain. It is difficult to devise quantitative in vivo methods, mainly because of the rapidity with which platelets adhere and aggregate in diseased or damaged blood vessels. Hypotheses for explaining in vivo platelet aggregation in biochemical terms must take the haemodynamic situation into account.