[Effect of hirudin on hormonally caused activation of nonenzymatic fibrinolysis in immobilization stress].
The specific inhibitor of thrombin-hirudin was used for studying the mechanism of activating effect of ACTH and adrenaline upon the unenzymatic fibrinolysis (UEF), the latter characterizing the function of the anticoagulating system (ACS). Simultaneous administration of ACTH and hirudin to animals subjected to the immobilization stress did not reduce the effect of ACTH upon UEF, while simultaneous administration of adrenaline and hirudin revealed a diminished effect of the former. This suggests different mechanisms of ACTH and adrenaline effects upon UEF: the stimulating effect of noradrenaline is realized through thrombinogenesis followed by activation of the ACS function and by an increase of UEF and therefore inhibitable by hirudin which form an inactive complex with thrombin. While the stimulating effect of ACTH upon UEF is exerted, apparently, not through thrombinogenesis and hence is valid even in presence of hirudin. Hirudin proper exerts no effect upon UEF.
D000324:Adrenocorticotropic Hormone; D000818:Animals; D004347:Drug Interactions; D004837:Epinephrine; D005341:Fibrinolysin / Q000037:antagonists & inhibitors; D005342:Fibrinolysis; D006629:Hirudins; D008297:Male; D051381:Rats; D012149:Restraint, Physical; D013312:Stress, Physiological / Q000097:blood* / Q000209:etiology; D014361:Trypsin Inhibitors
D006629:Hirudins; D014361:Trypsin Inhibitors; D000324:Adrenocorticotropic Hormone; D005341:Fibrinolysin; D004837:Epinephrine
Deĭstvie girudina na gormonal'no obuslovlennuiu aktivatsiiu nefermentativnogo fibrinoliza pri immobilizatsionnom stresse.