Parratt J R, Sturgess R M
Br J Pharmacol. 1977 Jun;60(2):209-19. doi: 10.1111/j.1476-5381.1977.tb07743.x.
1 In an attempt to investigate the possible role of released vasoactive substances in mediating the pulmonary pressor responses to E. coli endotoxin, cats were pretreated with histamine, 5-hydroxytryptamine (5-HT) or prostaglandin antagonists, with a histamine depleting agent (compound 48/80) or with an inhibitor of prostaglandin synthetase (sodium meclofenamate).2 The administration of endotoxin (2 mg/kg) resulted in a rapidly developing pulmonary hypertension (pressure twice normal after 2-3 min), increases in right atrial and intratracheal pressures, systemic hypotension and bradycardia. These effects were unaffected by methysergide in a dose sufficient to prevent the effects of intravenously administered 5-HT.3 Endotoxin responses were also unaffected by a combination of mepyramine and burimamide in doses sufficient to reduce markedly the effects of intravenously-administered histamine. In cats pretreated (chronically or acutely) with compound 48/80, endotoxin induced a transient pulmonary pressor response which was not maintained.4 The pulmonary and systemic responses to endotoxin were prevented by the prior administration of the prostaglandin antagonist, polyphloretin phosphate and by pretreatment with the prostaglandin synthetase inhibitor, sodium meclofenamate.5 It is concluded that a pulmonary vasoconstrictor prostaglandin is involved in the acute response to endotoxin in the cat.
为了研究释放的血管活性物质在介导大肠杆菌内毒素引起的肺升压反应中可能发挥的作用，对猫进行了预处理，分别给予组胺、5-羟色胺（5-HT）或前列腺素拮抗剂、组胺耗竭剂（化合物48/80）或前列腺素合成酶抑制剂（甲氯芬那酸钠）。
给予内毒素（2毫克/千克）导致迅速出现肺动脉高压（2 - 3分钟后压力升至正常的两倍）、右心房和气管内压力升高、全身性低血压和心动过缓。这些效应不受足以预防静脉注射5-HT作用剂量的麦角新碱的影响。
内毒素反应也不受足以显著降低静脉注射组胺作用剂量的甲氧苄胺嘧啶和布立马胺联合用药的影响。在经化合物48/80预处理（慢性或急性）的猫中，内毒素诱导出一种短暂的肺升压反应，但未能持续。
前列腺素拮抗剂多聚磷酸根皮苷预先给药以及用前列腺素合成酶抑制剂甲氯芬那酸钠预处理可预防对内毒素的肺和全身反应。
得出结论，一种肺血管收缩性前列腺素参与了猫对内毒素的急性反应。
