SUMMARY Over the past decade interest in and knowledge about the role of platelets in the haemostatic process and in various pathological conditions has continued to grow. The scope of laboratory methodology to investigate platelet function in clinical haemorrhagic and thrombotic disorders in the specialised haemostasis unit has also proportionally widened. After highlighting the physiological processes of the role of platelets in the haemostatic mechanism this brief review comments critically on the available routine techniques used to study platelet function in patients who present primarily with a bleeding tendency. Physiology of platelet function in haemostasisHaemostatic reactions can be classified into several overlapping and sequential events: localised vasoconstriction at the site of vessel injury: platelet adhesion to exposed subendothelial basement membrane and collagen fibres; formation of a platelet aggregate or plug; activation of the coagulation cascade leading to formation of fibrin, which reinforces the platelet plug; and finally, activation of the fibrinolytic system, which digests the haemostatic plug and allows growth of new vascular endothelial cells to complete the repair process.' Platelets circulate as non-nucleated discs and consist of a trilaminar phospholipoprotein membrane with submembrane circumferential contractile filaments, three types of granules, and an irregular internal network of canaliculi, through which the granule contents can be released on to the platelet surface.2The granule types are: dense granules which release adenosine diphosphate (ADP), adenosine triphosphate (ATP), serotonin, and calcium ions; a granules whose release constituents include platelet derived growth factor, platelet factor 4 with heparin neutralising ability, fi thromboglobulin, factor VIII related antigen/von Willebrand factor; factor V, fibrinogen, fibronectin, and probably thrombospondin; and lysosomal granules. Table 1 summarises the subsequent interactions with circulating platelets, which occur after damage to the vessel wall. When the vessel wall is damaged

Twelve female patients with severe secondary Raynaud's phenomenon were treated in a randomized order with both placebo and Iloprost infusions. Infusions were for 5 hours on 3 consecutive days and Iloprost was administered at variable dosage from 1.0 to 3.0 ng/kg/min. A 6-week follow-up period was used between the two sets of infusions. A significant number of patients reported Iloprost had improved Raynaud's symptomatology compared with placebo and this effect lasted for up to 6 weeks. The number of attacks of Raynaud's as recorded by patients in diary books was similarly reduced after Iloprost. Digital and nail-bed blood flows measured by laser-Doppler methods were increased for up to 6 weeks after Iloprost, but not after placebo infusions. Iloprost may be a useful therapeutic agent in the treatment of severe secondary Raynaud's syndrome.

ZK 36374 (Iloprost), a stable prostacyclin analogue, was administered to 6 healthy volunteers for 2-hour periods, with dose rates increasing from 0.5 to 2 ng/kg/min within that time. At these doses, which did not give troublesome side effects clinically, there was significant inhibition of ex vivo platelet aggregation responses to ADP and collagen. There was some rebound platelet hyperaggregability in all subjects, occurring between 1 and 2 h after termination of the infusion; this was of minor degree and was not associated with any clinical problems.

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