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Questions need for overt injury in thrombosis onset; leaves open human relevance and clinical translation.
Summary Aortas of mice, not exposed to any experimental injury, were examined by light and electron microscopy for the initial stages of mural thrombosis. Platelets in the lumen frequently formed groups or loose platelet aggregates. Individual platelets and platelet aggregates, both loose and dense, were often in contact with the inner vascular lining in focal areas. The underlying intimal tissue, including the endothelial cells, showed varying degrees of injury. Occasionally, however, platelet material was in contact even with structurally normal endothelial cells. The platelet- endothelial cell contact appeared to be an expression of adherence. Small mural thrombi were less frequently observed. They comprised platelets and fibrin and were mostly attached to subendothelial structures. Underneath the mural thrombi, the internal elastic membrane was often ruptured. The observed phenomena fit best with the theory that the primary event in mural thrombosis in aorta of mice is platelet aggregation under the influence of local flow irregularities. The next steps could be adherence of platelets to the vessel wall and injury of the intimai tissue through the release of vasodestructive agents from the platelets. Through this injury a focus of mural thrombosis could be established.
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Jørgensen et al. (1973) studied this question.
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