Goldblum S E, Wu K M, Tai H H
J Infect Dis. 1986 Jan;153(1):71-7. doi: 10.1093/infdis/153.1.71.
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.
血栓素（Tx）A2在肺炎链球菌诱导的粒细胞减少、血小板减少和肺白细胞淤滞中的作用尚不清楚。给兔子注射0.85%氯化钠、灭活肺炎球菌或在抑制TxA2合成酶预处理后注射灭活肺炎球菌。在注射前及注射后的不同时间点采集血液，进行粒细胞和血小板计数以及TxB2和6-酮前列腺素F1α（6-酮PGF1α）检测。通过组织学和生化方法（髓过氧化物酶活性）评估动物的肺白细胞淤滞情况。肺炎球菌攻击可导致显著的粒细胞减少（P<0.001）、血小板减少（P<0.001），TxB2（P<0.05）和6-酮PGF1α水平升高（P<0.001）以及肺白细胞淤滞（P<0.001）。抑制TxA2合成酶可阻断肺炎球菌诱导的TxB2水平升高，而不会显著改变循环粒细胞、血小板或6-酮PGF1α的水平。肺白细胞淤滞未被阻断。在另一组受肺炎球菌攻击的动物中，未发现TxB2或6-酮PGF1α有显著的跨肺梯度。
