: The effects of rapid
hemorrhage on coagulopathy have been reported. However, the effects of different
hemorrhage speeds on the blood coagulation/fibrinolysis system have not been investigated. This study aimed to compare different
hemorrhage speeds for clarifying their effects on the coagulation/fibrinolysis system and circulation disorders in rats. Male Sprague-Dawley rats (301-396 g) were randomly assigned to five groups depending on
hemorrhage speed and length of procedure: first, rapid (1.4 ml/min, 30-min
bleeding); second, rapid-L (1.4 ml/min, 30-min
bleeding and observation until 6 h); third, slow (0.1 ml/min, intermittently, 6-h
bleeding); fourth, control (30-min observation); and fifth, control-L (6-h observation).
Hemorrhage was induced by withdrawing blood until 40% of the estimated blood volume from the femoral artery. We measured vital signs, hematology, general chemistry, blood gas status, coagulation parameters, fibrinolytic markers [
tissue-type plasminogen activator and
plasminogen activator inhibitor one (PAI-1)], vascular endothelial damage (syndecan-1), and liver
PAI-1 mRNA expression. Rapid
hemorrhage induced elevation of
lactate and
syndecan-1 levels and prolonged prothrombin time and activated partial thromboplastin time in the rapid group. In contrast, slow
hemorrhage did not induce these changes.
Hemorrhage speed had no effect on plasma
tissue-type plasminogen activator and hematology. Plasma
PAI-1 levels were significantly increased in the rapid-L group, while liver
PAI-1 mRNA levels were increased in the slow group. This study shows changes in the circulatory and fibrinolysis systems, depending on the
hemorrhage speed.
Hemorrhage might promote production of
PAI-1, while tissue
hypoxia due to rapid
hemorrhage might promote release of
PAI-1.