Abstract
It is postulated that platelets are not produced by megakaryocyte budding within the bone marrow but by physical fragmentation in the pulmonary circulation. Alterations in the nature of the production site (the pulmonary vessels and their concomitant biochemical environment) or changes in the antecedent megakaryocyte cytoplasmic volumes with a concomitant. alteration in protein structure can produce platelets with a mean volume larger than normal. If such platelets are more reactive then they may be involved in atherogenesis and arterial thrombosis. Furthermore several pulmonary pathological states may arise from dysfunction during pulmonary platelet production.
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