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Intravenous infusions of one liter of low molecular weight and standard clinical dextran in normal adult subjects resulted in a significant alteration of platelet function as characterized by marked depression of platelet factor 3 (PF 3) activity. Disruption of the abnormal platelets by sonic oscillation corrected the defect, indicating that dextran coating of the platelets inhibited the release of PF 3 activity. These findings were confirmed by in vitro studies. Infusions of serum albumin failed to produce a significant alteration in PF 3 activity. The PF 3 depression could not be related to hemodilution or the total platelet count. Clot retraction, platelet adhesiveness, and the platelet thromboplastin test were normal. Serum prothrombin time was abnormal in some subjects. The platelet abnormality was related to the plasma dextran concentration and the retention of large dextran molecules in the circulation. Clinical dextran had a more deleterious effect on PF 3 activity than low molecular weight dextran. Since the majority of subjects had normal bleeding times associated with their reduced levels of PF 3 activity, the clinical significance of these studies is not clear. Nevertheless, the results of these experiments indicate that dextran coating of platelets interferes with the release of PF 3 activity, and suggest that alteration of the platelet surface may modify other platelet functions involved in maintaining a normal bleeding time.

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