Adhesion of platelets from 15 patients with von Willebrand's disease was tested in an ex vivo human umbilical vein model. Experiments employed umbilical veins still in their umbilical cords taken from patients undergoing cesarean section and platelets (fetal, adult and vW) either apyrase-washed or used as platelet-rich plasma or whole blood. F VIII R:Ag, F VIII:Rcof, and F VIII:C were measured in initial fresh plasma and in effluents from the umbilical vein segments. F VIII:Rcof increased in most perfusates. Binding of latex-linked specific antihuman F VIII R:Ag demonstrated that F VIII R:Ag existed on subendothelium and on injured endothelial cells. Scanning electron microscopy three-dimensionally displayed vW platelet--vessel-wall interactions. Although vW platelets adhered to injured vein, both qualitative and quantitative differences existed in comparison with adhesion of normal platelets. The differences correlated best with the plasma F VIII:Rcof level. The best adhesion shown by vW platelets was only 51 percent of the adhesion of control fetal or adult platelets. vW platelets had less surface activity, fewer pseudopods, and little ability to spread and pave the exposed subendothelium. Pretreatment of the vein with F VIII R:Ag antibody partly blocked adhesion. Coperfusion of cryoprecipitate with vW platelets improved their adhesivity, state of activation on subendothelium, and ability to form aggregates. ABO differences in blood cell types of fetal material and platelet donors seemed without effect, which further establishes this model's validity for studies of platelet dysfunction and platelet or endothelial reactive agents.