I. Conclusions
Injury to vessels leads to the formation of platelet plugs and fibrin clots. For nearly
a century it has been known that these mechanisms stop bleeding and may produce thrombi.
They may be triggered by trivial trauma (180), and hemostasis possibly occurs in one
or more vessels at all times in the normal body. The blood is capable of removing
at least the fibrin part of such deposits; however, some of them may progress into
arteriosclerotic lesions (59). The accumulated evidence, therefore, supports the concept
of a hemostatic balance on the local level, triggered by an abnormal local factor.
In this review, however, we are concerned with a general and continuous hemostasis which takes place on the normal, uninjured endothelium. Direct examinations have
suggested that hemostatic products are present on normal endothelium, but these investigations
cannot be accepted as conclusive. Much of the indirect evidence is weak or controversial.
However, the purpura and increased capillary fragility in platelet disorders strongly
suggest that platelets are important for vascular integrity, and animal experiments
suggest that both platelets and coagulation influence vascular permeability. At present,
therefore, the theory of continuous hemostasis can neither be accepted nor rejected;
further evidence must be collected.
