Some interactions between human platelets and glass: von Willebrand's disease compared with normal.

Abstract

If native or heparinized blood is passed slowly through a column of glass beads at room temperature, the number of platelets removed from the initial drop emerging from the column is less than that removed from the final drop. At 4 degrees C. this difference disappears. If the blood is passed rapidly through such columns at room temperature fewer platelets are removed, but the initial-final difference persists. Von Willebrand's platelets are removed normally at slow speeds; at fast speeds abnormally few platelets are removed. Platelets emerging from all such columns are in aggregates. On adding glass beads to normal heparinized plasma, the platelets at once become more rounded and after about 50 seconds' delay they aggregate: the delay and rate of aggregation can be quantitated. Aggregation occurs best at 20 to 30 degrees C. and is not inhibited by the addition of some enzyme inhibitors. In von Willebrand's disease all these glass-induced aggregation phenomena occur normally and aggregation in response to adenosine diphosphate (ADP), serotonin creatinine sulphate (5-HT), adrenaline, collagen, and glass is also normal.