Hereditary Defect in Platelet Function in Rats

Low values in Hemostatic parameters of fawn-hooded rats with an inherited hemorrhagic diathesis suggest the absence of the platelet, "release pool" rather than a defective release mechanism.

Abstract

Abstract Hemostatic parameters of fawn-hooded (FH) rats with an inherited hemorrhagic diathesis were compared with those of normal rats. Prothrombin time, partial thromboplastin time, plasma factor VIII, plasma fibrinogen, and platelet count and volume were normal. Bleeding time (BT) in FH rats was over 15 min vs. 1-8 min in controls, and platelet retention in glass-bead columns was reduced. Transfusion of platelet concentrates from normal rats corrected the BT of thrombocytopenic FH rats, but FH rat platelets did not shorten the BT of thrombocytopenic controls. ADP-induced aggregation, measured turbidimetrically in heparinized FH platelet-rich plasma, was normal. Connective tissue did not aggregate platelets of FH rats and released a subnormal amount of 14C-serotonin. In comparison with control platelets washed FH platelets aggregated by thrombin released virtually no ATP and ADP. Platelets, 10,11 of normal rats contained 4.49 µmoles ATP, 0.98 µmoles ADP, and 0.88 µmoles serotonin compared with only about one-half as much ATP and ADP and one-third as much serotonin in platelets of FH rats. These low values suggest the absence of the platelet, "release pool" rather than a defective release mechanism. The hemorrhagic diathesis seen in the FH rats resembles the platelet defect with storage pool deficiency observed in man.2