Active translocation of platelets into sinusoidal and Disse spaces in the liver in response to lipopolysaccharides, interleukin-1 and tumor necrosis factor.

1. Injection of lipopolysaccharides (LPS) or endotoxin into mice and rats induces a prolonged increase in serotonin (5-hydroxytryptamine: 5HT), predominantly in the liver. 2. The 5HT increase reflects the accumulation of platelets in the sinusoidal and perisinusoidal Disse spaces (spaces between endothelial cells and hepatocytes) in the liver. 3. Most of the platelets which accumulated in these spaces still retained their intact structure and a large amount of 5HT. 4. Interleukin-1 and/or tumor necrosis factor also induce the platelet response. 5. Kupffer's cells play a key role in this platelet response. 6. Anti-platelet drugs currently used, except for anti-inflammatory steroids, were ineffective in preventing the platelet response. 7. This platelet response is different from the well known platelet aggregation. 8. The possible involvement of this platelet response in insulin-independent hypoglycaemia, disseminated intravascular coagulation, septic shock, hepatitis, Shwartzman type reactions or self-defense mechanisms is discussed.