Platelet life span in normal, splenectomized and hypersplenic rats.

destruction, and the increased platelet level following splenectomy might be due to a decreased destruction of platelets. Likewise, the decreased level in hypersplenism might be due to an increased destruction. One approach to this problem is to label platelets in vitro, and then study their localization in the normal animal. The spleen contains a considerable amount of the label in such experiments,14 apparently supporting the concept that the spleen normally destroys a large fraction of platelets. However, this evidence may be criticized on the grounds that in vitro labeling and handling may damage the platelets and lead to abnormal tissue localization. The body may handle its own intact platelets differently. Another approach to the problem is to study the possible influence of the spleen on the platelet life span by in vivo tagging. If the spleen is the main destructor of platelets, their life span might be prolonged after splenectomy, all(l shortened in hypersplenism. Following this approach, we have found the platelet life span to be the same in normal, splenectomized, and hypersplenic rats.