Experimental Hemostasis in Normal Dogs and Dogs with Congenital Disorders of Blood Coagulation

Hemostasis was examined after transection of vessels, 50-200 microns in diameter, both in normal dogs and in dogs with congenital defects of either factor VII, factor IX, or factor VIII. The formation of the hemostatic platelet plugs was observed by direct microscopy in vivo, and sections of the plugs were prepared for both light and electron microscopy 10 to 30 minutes after transection. Furthermore, the reaction of platelets from normal and abnormal dogs with adenosine diphosphate, collagen and thrombin was tested in vitro by a turbidimetric technic.

In normal and factor VII deficient dogs the initial arrest of bleeding took place about 3 minutes after transection, and rebleeding was infrequently observed. Their platelet plugs were composed of densely packed platelets, anchored to the vascular and perivascular tissue and surrounded by a cap of fibrin.

In factor IX deficient dogs there was no definite prolongation of the initial bleeding time, but rebleedings were frequent. In factor VIII deficient dogs the initial bleeding time was prolonged and the intensity of the bleeding had a wave-like characteristic. The plugs in the hemophilic dogs were larger than normal, were rich in channels, and had areas of loosely packed platelets and an incomplete fibrin cap.

Treatment of factor IX deficient dogs with Dicumarol did not further impair hemostatic plug formation in the doses used. Treatment of factor VII deficient dogs with heparin, or factor IX deficient dogs with phenylbutazone, prolonged the bleeding time markedly, delayed the building up of the plug, and gave fragile, loosely packed plugs. Treatment of normal dogs with phenylbutazone did not alter the hemostatic process at the dosage used.

In the in vitro studies, platelets from the dogs with congenital coagulation defects reacted normally with the aggregating stimuli.

It is concluded that the initial platelet interaction wih the vessel wall and surrounding tissue is not dependent upon blood coagulation. An intact intrinsic pathway of coagulation is necessary for the stabilization of the hemostatic plug after it is formed.