Abstract
Abstract 1. Small amounts of thromboplastin intravenously cause platelet sequestration. This is followed by fibrinogen sequestration. Large doses of intravenously administered thromboplastin lead to irreversible destruction or utilization of platelets and fibrinogen. 2. The following theories are advanced: (a) This platelet sequestration may be due to platelet clumping caused by coagulation occurring on the platelet surface. Surface coagulation may be initiated by the action of thromboplastin or thrombin on the plasma proteins and calcium adsorbed on the platelet surface. The platelet clumps may be filtered out in the sinusoidal spaces of the body, especially in liver and spleen. (b) The coagulation on the platelet surface may lead to partial polymerization of the fibrinogen molecule. (c) As long as this polymerization is reversible, the entire process remains reversible. When polymerization proceeds far enough so as to become irreversible, the platelets and fibrinogen can no longer return to the circulation. (d) This same mechanism may explain other examples of platelet sequestration.
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