Release of thromboplastin after thermal injury.

Abstract

SummaryMicrocirculatory flow following a severe burn is hindered by the formation of aggregates of erythrocytes which frequently completely fill the lumena of small arteries, arterioles, and venules. On the arterial side, clusters of cells are often too large to enter branching vessels; large aggregates grow from smaller clusters, and vessels fill with packed, adherent erythrocytes for some distance proximal to divarications. However, if erythrocytes enter capillaries, they move independently of other erythrocytes and are transformed into hollow paraboloids as they are in the absence of trauma to tissue or in the absence of infused thromboplastin.The hypothesis that aggregation of erythrocytes is caused either directly or indirectly by release of thromboplastins from damaged tissue is based upon the following evidence:1) Following a severe burn the observed phenomena in cinephotographic film recorded at conventional film speeds and up to 3200 frames per sec, are similar to those observed following the infusion of thromboplastin.2) Changes in clotting and fibrinolytic components following a severe burn can be duplicated by the infusion of canine thromboplastin. The most pronounced alteration is the shortening of the Stypvin time which is highly dependent upon the concentration of phospholipids.3) Complete fibrinogenolysis results in improvement in microcirculatory flow following a severe burn and following the infusion of thromboplastin, indicating that an altered fibrinogen, or possibly fibrin, is involved in the adherence between erythrocytes in both experimental conditions.