The role of the heart in the mechanism modifying the functional state of the blood clotting and fibrinolytic systems in thyroxine toxicosis.
In 36 rabbits the role of the heart in the genesis of changes in the tissue components of blood clotting and fibrinolysis in thyroxine toxicosis was studied. It was found that on the 5th and 10th days of toxicosis the thromboplastic (P = 0.002) an anticoagulant (P less than 0.001) myocardial activities decreased, and on the 15th day, increased. On the 20th day the myocardial thromboplastic activity remained increased, whereas the anticoagulant activity was further sinking (P = 0.05). Simultaneously the total fibrinolytic activity in the blood flowing through the heart and in myocardial extract increased (P less than 0.001), and the antiplasmin activity decreased.
D000818:Animals; D001777:Blood Coagulation; D005260:Female; D005342:Fibrinolysis; D006321:Heart / Q000503:physiopathology*; D006493:Heparin / Q000502:physiology; D008297:Male; D010958:Plasminogen / Q000502:physiology; D011817:Rabbits; D013918:Thrombin Time; D013974:Thyroxine / Q000633:toxicity*; D000979:alpha-2-Antiplasmin / Q000502:physiology
D000979:alpha-2-Antiplasmin; D010958:Plasminogen; D006493:Heparin; D013974:Thyroxine