Piper P J
Eur J Respir Dis Suppl. 1983;129:45-64.
Leukotrienes (LTs) are generated from human and guinea-pig lung tissue during antigen challenge. Both human and guinea-pig lung generate LTD4, LTC4, and LTE4 are also formed by human lung and LTB4, by guinea-pig lung. LTC4, LTD4, and LTE4 contract guinea-pig trachea and human bronchus, LTC4 and LTD4 being very much more active than histamine. LTB4 shows some activity but rapidly develops tachyphylaxis. In preparations of guinea-pig lung (perfused lung and parenchymal strips) all LTs cause stimulation of a phospholipase and release of thromboxane A2 (TxA2) and other cyclo-oxygenase products. TxA2 is bronchoconstrictor and augments the LT-induced contractions of guinea-pig parenchyma. Contractions of parenchyma are inhibited by indomethacin, carboxyheptylimidazole or mepacrine. LTs are much less active in contracting parenchymal tissue from human, rat or rabbit and there is no evidence of LT-induced release of TxA2 in these tissues. Since LTC4 and LTD4 cause coronary vasoconstriction in guinea-pig or rat isolated hearts and greyhounds in vivo, LTs generated in lung during antigen challenge may contribute to anaphylactic cardiac depression. LTC4 and LTD4 cause vasoconstriction in guinea-pig skin and constrict guinea-pig pulmonary artery. Recently we have shown that LTs are generated from selected arteries by immunological and non-immunological stimulation. Pulmonary (pig, human, guinea-pig) and coronary arteries (pig) produced the highest concentration of LTD4-like material. The generation of LTs by and their possible actions on the pulmonary circulation may be important in respiratory disease. LTs, B4, C4, D4 cause exudation of plasma (sometimes potentiated by prostaglandins) in the skin of various species. If LTs have similar actions in the lung they may contribute to oedema of the airways. LTC4 is a weak stimulator of mucin secretion in cat trachea but may synergise with prostaglandins released in allergic conditions.
在抗原激发过程中，白三烯（LTs）由人和豚鼠的肺组织产生。人和豚鼠的肺都能产生LTD4，人肺还能形成LTC4和LTE4，豚鼠肺则能产生LTB4。LTC4、LTD4和LTE4可使豚鼠气管和人支气管收缩，LTC4和LTD4的活性比组胺高得多。LTB4有一定活性，但很快会产生快速耐受性。在豚鼠肺的制备物（灌注肺和实质条）中，所有白三烯都会刺激磷脂酶并释放血栓素A2（TxA2）和其他环氧化酶产物。TxA2是支气管收缩剂，会增强白三烯诱导的豚鼠实质收缩。实质收缩可被吲哚美辛、羧基庚基咪唑或米帕林抑制。白三烯在收缩人、大鼠或兔的实质组织时活性低得多，且没有证据表明白三烯能在这些组织中诱导TxA2释放。由于LTC4和LTD4在豚鼠或大鼠离体心脏以及灵缇犬体内会引起冠状动脉收缩，抗原激发时肺中产生的白三烯可能导致过敏性心脏抑制。LTC4和LTD4会使豚鼠皮肤血管收缩并使豚鼠肺动脉收缩。最近我们发现，通过免疫和非免疫刺激，特定动脉也能产生白三烯。肺（猪、人、豚鼠）和冠状动脉（猪）产生的LTD4样物质浓度最高。白三烯的产生及其对肺循环的可能作用在呼吸系统疾病中可能很重要。白三烯B4、C4、D4会导致各种物种皮肤血浆渗出（有时会被前列腺素增强）。如果白三烯在肺中有类似作用，它们可能会导致气道水肿。LTC4是猫气管中粘蛋白分泌的弱刺激剂，但可能与过敏状态下释放的前列腺素协同作用。
