The purpose of this study was to identify mechanisms responsible for the thrombocytopenia that accompanies gram-negative septicemia. Fifty-one piglets, 4 hours to 21 days old, were studied. Experimental animals were injected intra-arterially with live E. 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 megakaryocyte number, nuclear generations, or morphology. There was a steady decrease in platelet aggregation to adenosine diphosphate (ADP), increasingly severe disruption of the morphology of the circulating platelets by electron microscopy, and a moderate increase in the number of circulating platelet aggregates in animals infused with E. coli. No platelet aggregates were observed to be occluding microcirculatory vessels. Small vessels in one third of the pulmonary parenchyma frequently were obstructed by masses containing erythrocytes, leukocytes, platelets, and fibrin. Single platelets were seen to be adherent to the lining of blood vessels. The architecture of platelets making up aggregates and of 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. It was concluded that 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.
|Original language||English (US)|
|Number of pages||7|
|State||Published - Dec 1 1978|
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