论文部分内容阅读
10年前已证实血管紧张素转换酶抑制剂(ACEI)能引起咳嗽,其产生机制尚不清楚。有研究认为,ACEI能抑制缓激肽分解代谢,使组织内及支气管内缓激肽浓度增加,直接刺激迷走神经C纤维引起咳嗽,也可能间接刺激磷酯酶A2,激活花生四烯酸,增加前列腺素合成而引起。花生四烯酸代谢产物不仅包括前列腺素,还包括前列环素和血栓烷(TX)。后者是强有力的血管收缩剂及血小板聚集剂。吡考他胺(Picotamide)是一种抗血小板聚集剂,并能抑制TX合成并拮抗TX/PGH受体。但对环氧酶不产生活性作用。作者为评价ACEI引起的咳嗽是否伴有TX合成增加和切断TX经路后是否能缓解咳嗽进行随机双盲交叉研究。
10 years ago, angiotensin converting enzyme inhibitor (ACEI) has been proven to cause cough, the mechanism of its production is not clear. Some studies suggest that, ACEI can inhibit bradykinin catabolism, bradykinin and intra-bronchial tissue concentration increased, directly stimulate the vagus nerve C fibers cause cough, may also indirectly stimulate phospholipase A2, activate arachidonic acid, increase prostate Su lead to synthesis. Arachidonic acid metabolites include not only prostaglandins but also prostacyclin and thromboxane (TX). The latter is a powerful vasoconstrictor and platelet aggregation agent. Picotamide is an anti-platelet aggregation agent that inhibits TX synthesis and antagonizes TX / PGH receptors. But does not produce the active role of epoxidase. The authors randomized double-blind crossover study to evaluate whether ACEI-induced cough is accompanied by an increase in TX synthesis and whether the TX pathway is severed after cough relief.