No abstract

Traumatized rat omentum was used to demonstrate the development of "platelet plugs" following agitation in platelet-rich plasma. In the absence of divalent cation there was only platelet adhesion to connective tissue fibers; in the presence of divalent cation masses of platelets formed (cohesion) even in plasma adequately anticoagulated with heparin. Exposure of these platelet masses to thrombin produced greater compactness and stability. Human and rat platelets behaved alike with the traumatized rat omentum; platelets from two patients with von Willebrand's disease gave normal reactions whereas platelets from a patient with thrombasthenia showed adhesion only. Exposure of human platelets to washed connective-tissue fragments or to thrombin elicited clumping accompanied by release of serotonin and of adenine nucleotides (AN) of which about one-third was adenosine diphosphate. Intermediate concentrations of connective tissue and thrombin also caused clumping but no liberation of AN or serotonin. ADP caused intense clumping but failed to liberate serotonin or additional ADP. It is suggested that cohesion reaction is mediated by release of ADP. The traumatized omentum appears to be a suitable model for studying the hemostatic process.

A family is reported with multiple cases of neonatal neutropenia. The first child died of severe infection, the second was asymptomatic, the third and the fourth children had a benign course of agranulocytosis which lasted about 10 weeks and was followed by spontaneous recovery. A potent leukoagglutinin was found in the maternal serum which agglutinated leukocytes obtained from the father and all three available children but failed to agglutinate the mother’s own cells. Identical leukoagglutinin was found in the last baby’s serum; it disappeared after the baby recovered. The disorder is tentatively named "isoimmune neonatal neutropenia" and is considered to represent a condition analogous to erythroblastosis fetalis.