To examine the platelet aggregating activity in a physiological condition, we studied the spontaneous platelet aggregation in whole blood without adding platelet aggregating agents. The spontaneous aggregating rate was determined by the drop in the number of single platelets counted with a Coulter Counter.
The spontaneous aggregation of normal platelets was increased in proportion to the increment in the stirring rate. We examined the aggregating rate 30 minutes after starting stirring at 500rpm, as the reproducibility was rather satisfactory at this condition. An increment in the aggregation was found in the existence of red blood cells (RBC) (than the condition without RBC.) The inhibition effects to platelet aggregation of dilazep possessing the stabilizing activity of RBC membranes was stronger than that of aspirin. These results suggest that the presence of RBC considerably affects those reactions. In order to remove the effect of ADP from RBC, creatine phosphate and creatine phosphokinase (CP/CPK) were added into this reaction. However this did not inhibit this reaction completely. When both CP/CPK and aspirin were added together, the reaction was not completely inhibited. This suggests the existence of different aggregation mechanism than ADP and thromboxane A2.
This aggregating rate was significantly higher in patient with DM compared with the control group. These results indicate that the spontaneous platelet aggregating rate in whole blood is valuable for determining platelet hyperfunction.
