Affiliations: Department of Haematology, The Medical School, University of Birmingham, Birmingham | Bioengineering Unit, Strathclyde University, Glasgow, UK
Note: [] Current Address: 3rd Department of Medicine, Jikei University School of Medicine, 3-25-8 Nishi Shinbashi, Minato-Ku, Tokyo 105, Japan.
Abstract: Interaction between platelets and granulocytes may contribute to ischaemic and inflammatory disorders. We have used a recently developed granulocyte aggregation assay, in which isolated granulocytes and platelet-rich plasma (PRP) are mixed, to test the ability of a range of pharmacological agents to inhibit this interaction. A stable prostacyclin analogue (Iloprost) could completely inhibit platelet-induced granulocyte aggregation if the whole blood was treated immediately following withdrawal, but not if the agent was added to granulocytes or PRP after isolation. A surfactant (Poloxamer 188) added to the whole blood, either increased aggregation or had no effect, depending on the source of the compound under test. Naftidrofuryl oxalate and pentoxifylline tended to reduce aggregation, but these effects were not statistically significant. It appears that agents which can inhibit platelet activation may reduce adhesion to granulocytes, but are unable to reverse the interaction after the platelets have been stimulated.
