Abstract
Activation of heparin secretion by connective tissue mast cells under conditions of immobilization stress is determined by activation of the sympathoadrenal system, secretion of adrenocorticotropic hormone, and possible generation of thrombin. Generation of thrombin in the blood under these conditions is confirmed by a significant drop in the proenzyme protein C concentration by 23%, a decrease in the activity of factor V (substrate of protein C) by 36%, and prolongation of activated partial thromboplastin time by 40%. It is shown that 30-min immobilization leads to a 3-fold depletion of the heparin pool in mast cells. Intravenous injection of hirudin, a specific thrombin inhibitor, before immobilization slightly diminishes the stimulating effect of stress on heparin secretion. These data suggest that apart from catecholamines and adrenocorticotropic hormone, thrombin generated in the bloodstream during stress also markedly contributes to activation of heparin secretion by mast cells.
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