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休克并发急性呼吸衰竭时血中5-羟色胺(5-HT)增高,造成肺血管收缩,增强儿茶酚胺和血管紧张素对血管的作用,从而形成肺动脉高压。5-HT还可造成支气管收缩和血小板聚集。动物实验表明,输注5-HT后观察到的肺水肿是继肺微血管压增高而发生的。 Ketanserin是喹唑啉的衍生物,能特异性地抑制血管、气管和血小板的5-HT_2受体。最近在肺栓塞动物实验中观察到Ketanserin能抑制肺动脉压增高并能减少肺分流。研究还证实,此药使肺血管系统恢复原状,可能使肺血管扩张并使已聚集的血小板恢复正常。这些效应对治疗急性呼吸衰竭也可能有价值,因为急性呼吸衰竭时很可能有肺微血栓形成。本文目的是调查Ketanserin治疗急性呼吸衰竭的作用和对血流动力的影响。
Shock with acute respiratory failure in the blood 5-hydroxytryptamine (5-HT) increased, causing pulmonary vasoconstriction, increased catecholamine and angiotensin on the blood vessels, resulting in pulmonary hypertension. 5-HT can also cause bronchoconstriction and platelet aggregation. Animal experiments have shown that pulmonary edema observed after infusion of 5-HT is associated with increased pulmonary microvascular pressure. Ketanserin is a quinazoline derivative that specifically inhibits 5-HT 2 receptors in blood vessels, trachea and platelets. Recently, it has been observed in animal experiments of pulmonary embolism that Ketanserin inhibits increased pulmonary artery pressure and reduces pulmonary bypass. The study also confirmed that this drug restores the pulmonary vasculature and may cause pulmonary vasodilation and return of aggregated platelets. These effects may also be of value in the treatment of acute respiratory failure, as pulmonary microthrombus formation is most likely to occur during acute respiratory failure. The purpose of this article is to investigate the effects of Ketanserin in the treatment of acute respiratory failure and its effects on hemodynamics.