Eighty-seven patients with complicated patterns of peptic ulcer were examined for different components of the hemostatic system including gastric and duodenal fibrinolysis. It was established that the penetrating ulcer gives rise to hypocoagulemia and accelerates fibrinolysis. The perforating and hemorrhagic ulcers are associated with hypercoagulation, which is a manifestation of the stress response of the body. It is shown that gastric juice and the duodenal content have a hypocoagulation (heparinoid) action on blood and plasma coagulation. Peptic ulcer is marked by high gastric and duodenal fibrinolysis and proteolysis both in the gastric and duodenal mucosa and in the free gastric and duodenal contents as well. It is postulated that all the factors under consideration, which are unfavourable for local hemostasis, may be involved in the pathogenesis of gastroduodenal hemorrhages. The author holds that hemostatics, which suppress fibrinolysis and the acid-peptic factor and stimulate blood coagulation and clot formation in the zone of hemorrhage, may be used locally.