Role of neutrophils and platelets in the pathogenesis of focal hepatocellular necrosis in endotoxaemia

Summary To clarify whether neutrophils and platelets are implicated in the pathogenesis of focal hepatocellular necrosis in endotoxaemia, we examined the relationship between the changes in neutrophils and platelets in peripheral blood and the degree of focal hepatocellular necrosis and serum transaminase activity in rats after endotoxin injection. The number of neutrophils in the peripheral blood decreased rapidly during the first hour after endotoxin injection and then increased. This initial decrease might be caused by the adhesion of neutrophils to pulmonary capillary walls, and the subsequent increase might be caused by granulocyte colony-stimulating factor mediated by endotoxin. However, there was no relationship between the degree of focal hepatocellular necrosis and the number of neutrophils sticking to the walls of hepatic sinusoids or the changes in the neutrophil count in the peripheral blood. The number of platelets in the peripheral blood decreased rapidly after endotoxin injection. There was a statistically significant relationship between the number of platelets in the peripheral blood and the level of serum transaminase activity: the fewer the platelets, the more severe was focal hepatocellular necrosis. The present study suggests that rapid and extensive consumption of platelets, rather than neutrophils sticking to the sinusoidal walls, is involved in the pathogenesis of focal hepatocellular necrosis in endotoxaemia.