Stress is involved in the development of diseases related to abnormal hemostasis. Thrombosis may develop whenever the dynamic balance be- tween prothrombotic and antithrombotic processes become altered. Recently, renin angiotensin system is considered to be a stress hormone response system The aim of the present work was to clarify the effect of acute and chronic stress on the prothrombotic and antithrombotic activity and to study the role of angiotensin II in these stress-induced changes. The results of this work showed that acute ether stress and chronic isola- tion stress lead to suppression of both intrinsic and extrinsic coagulability manifested by a decrease in the jibrinogen concentration and a decrease in the activity of factors VH and X, at the same time acute and chronic stress caused a decrease in the antithrombotic activity indicated by a re- duction in the activity of antithrombin III. This means that hemostatic bal- ance is probably maintained at a low level, this make it difficult to hypothesize the existence of a hypercoagulable or a hypocoagulable state during stress. These changes can not be attributed to hemodilution since we found that stress causes hemoconcentration indicated by increased packed cell volume. The results of this work showed, also, that, these stress-induced hemostatic changes was prevented by pretreatment with the angiotensin converting enzyme inhibitor (perindopril), this means that these stress—induced hemostatic changes is mediated, at least partially, through the renin angiotensin system. |
