SummaryA simple method for quantitating pletelet adhesiveness to glass is described. The use of minimally manipulated native whole blood and direct counting of adherent platelets are principal features of the method. Normal values for platelet adhesiveness to glass both in the absence and presence of added ADP are given. Without ADP, abnormally low platelet adhesiveness values were observed in afibrinogenemia, thrombasthenia, uremia, homocystinuria and in some patients with von Willebrand’s disease or Hageman trait. Under the same test condition, abnormally elevated values were found in some patients with von Willebrand’s disease or diabetes mellitus. With added ADP, which induced aggregation of some platelets in the blood, abnormally low platelet adhesiveness values were observed in thrombasthenia and one diabetic patient, while abnormally high values were found in von Willebrand’s disease, and in one patient with homocystinuria. The test for platelet adhesiveness performed with added ADP may have diagnostic value for patients with von Willebrand’s disease.

SummaryA correlation between effects of a series of compounds on platelet adhesion, aggregation, and retraction of the clot, and their effects on platelet electrophoretic mobility, ecto-ATPase activities, and AChE activity has been sought. Compounds which inhibited aggregation induced by ADP or epinephrine also inhibited platelet adhesion to glass. Six compounds which inhibited adhesion and aggregation did not inhibit clot retraction. The data suggest that the effect of thrombin on platelet electrophoretic mobility and ecto-ATPase activities may have less influence on platelet function than was formerly believed. However, the effects of test compounds on platelet AChE activity suggest that this enzyme may play a role in aggregation and adhesion. Platelet adhesion and aggregation may operate by similar mechanisms.

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