Summary
Venous stasis occurs when people are at bedrest, because of altered venous flow characteristics.
This is commonly believed to be one etiology behind the development of deep venous
thrombosis (DVT). The hemostatic effects of bedrest and their possible role in DVT
development have not been fully examined. We hypothesized that bedrest would lead
to increases in hemostatic function and that these increases could be important in
the development of DVT.
Twelve non-smoking volunteers were studied during supine positioning for 36 hours.
Platelet reactivity and plasma concentrations of fibrinogen, a2-antiplasmin, plasminogen,
thromboxane (32, plasminogen activator inhibitor-1, tissue plasminogen activator and
neuroendocrine hormones (cortisol, epinephrine and norepinephrine) were measured at
8:00 a.m., 10:00 a.m., 4:00 p.m. and 8:00 a.m.
Cortisol demonstrated an early morning increase while catecholamines were unchanged
throughout. Fibrinogen, a2-antiplasmin, plasminogen and platelet reactivity were no
different at any time point. Fibrinolytic proteins changed over time, manifested by
decreased PAI-1 antigen and activity levels at 24 h.
Based upon the parameters measured, bedrest causes no increase in hemostatic function.
In fact, bedrest causes the potential for enhanced fibrinolysis, that differs from
that previously reported for normal activity over 24 h. This may represent a protective
mechanism to counter the effects of stasis from bedrest.
