Thromboxane as a mediator of pulmonary dysfunction during intravascular complement activation in sheep.
Thromboxane as a mediator of pulmonary dysfunction during intravascular complement activation in sheep.
复制标题
血栓烷作为绵羊血管内补体激活过程中肺功能障碍的介质。
DOI：
10.1164/arrd.1986.133.2.269
复制
发表时间：
1986
期刊：
影响因子：
--
通讯作者：
Wasserman,MA
中科院分区：
文献类型：
--
作者：
Gee,MH;Perkowski,SZ;Tahamont,MV;Flynn,JT;Wasserman,MA
Intravascular complement activation results in thromboxane (TxA2) production, pulmonary hypertension, hypoxemia, and increased lung vascular permeability. The purpose of this study was to determine the role of TxA2as a mediator of these responses. Experiments were made in anesthetized sheep subjected to intravenous injections of zymosan-activated plasma (ZAP) every 30 min for 4 h. Sheep were pretreated with dazoxiben, a TxA2synthetase inhibitor, or SK and F 88046, a TxA2end-organ antagonist, and the results were compared with those from untreated sheep. Dazoxiben, but not SK and F 88046, inhibited TxA2release. The hypertensive response averaged 74 ± 3 cm H2O after each injection of ZAP in untreated sheep. Neither drug altered this response. Pao2decreased an average of 20 ± 1 mmHg in untreated sheep, 3 ± 1 mmHg in dazoxiben-treated sheep, and 11 ± 1 mmHg in SK and F 88046−treated sheep. Increases in lung lymph flow and lymph protein clearance were unaffected by treatment. TxA2appears to be an important mediator of hypoxemia during intravascular complement activation.
