Streptococcus pneumoniae-induced alterations in levels of circulating thromboxane and prostacyclin: dissociation from granulocytopenia, thrombocytopenia, and pulmonary leukostasis.

The role of thromboxane (Tx) A2 in Streptococcus pneumoniae-induced granulocytopenia, thrombocytopenia, and pulmonary leukostasis is unclear. Rabbits were injected with 0.85% NaCl, nonviable pneumococci, or nonviable pneumococci after pretreatment with TxA2 synthetase inhibition. Blood was obtained immediately before and at times after injection for granulocyte and platelet counts and assays of TxB2 and 6-keto prostaglandin F1 alpha (6-ketoPGF1 alpha). Animals were evaluated for pulmonary leukostasis histologically and biochemically (myeloperoxidase activity). Pneumococcal challenge induced significant granulocytopenia (P less than .001), thrombocytopenia (P less than .001), and elevations in levels of both TxB2 (P less than .05) and 6-ketoPGF1 alpha (P less than .001) as well as pulmonary leukostasis (P less than .001). TxA2 synthetase inhibition blocked the pneumococcus-induced elevation in level of TxB2 without significantly altering levels of circulating granulocytes, platelets, or 6-ketoPGF1 alpha. Pulmonary leukostasis was not blocked. In another group of pneumococcus-challenged animals, no significant transpulmonary gradients of either TxB2 or 6-ketoPGF1 alpha were found.