The mechanisms of thrombocytopenia in experimental gram-negative septicemia
Rowe, M.I.; Marchildon, M.B.; Arango, A.; Malinin, T.; Gans, M.A.
Surgery 84(1): 87-93
1978
ISSN/ISBN: 0039-6060 PMID: 351840 Document Number: 135957
Fifty-one piglets, 4 h to 21 days old, were studied to identify mechanisms responsible for the thrombocytopenia that accompanies gram-negative septicemia. Experimental animals were injected intra-arterially with live Escherichia coli, and control animals with normal saline solution. Animals injected with bacteria had a progressive fall in platelet count to preinjection levels. No differences were found between experimental and control piglets in megakaryocytes number, nuclear generations or morphology. There was a steady decrease in platelet aggregation to ADP, increasingly severe disruption of the morphology of the circulating platelets by EM and a moderate increase in the number of circulating platelet aggregates in animals infused with E. coli. No platelet aggregates were observed occluding microcirculatory vessels. Small vessels in 1/3 of the pulmonary parenchyma frequently were obstructed by masses containing erythrocytes, leukocytes, platelets and fibrin. Single platelets were adherent to the lining of blood vessels. The architecture of platelets making up aggregates and those adherent to blood vessels had relatively well-preserved ultrastructure. The platelet responses and light and electron microscopic findings after injection of E. coli were similar in splenectomized and nonsplenectomized animals and newborn and maturing piglets. The thrombocytopenia that developed in response to the injection of live E. coli was due primarily to platelet injury and destruction and only platelets that were relatively intact functionally and morphologically took part in aggregation and adhesion.