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. Re
cently, renin angiotensin system is considered to be a stress hormone re
sponse 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 fibrinogen concentration and a decrease
in the activity of factors VII 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 hy -
pothesize 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 |
