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目的：探讨内源性速激肽是否参与抗原诱导的豚鼠心血管反应。方法：观察速激肽ＮＫ－１受体拮抗剂ＣＰ－９６３４５对ｉｖ抗原（卵白蛋白，ＯＡ）或Ｐ物质（ＳＰ）引起致敏豚鼠血压变化及不同组织伊文思蓝渗出的影响。结果：ＯＡ（５ｍｇ·ｋｇ－１）或ＳＰ（２μｇ·ｋｇ－１）均引起麻醉豚鼠血压降低；支气管、肺内气道、心房、心室、耳廓和膀胱的伊文思蓝渗出增加。ＣＰ－９６３４５（０．３，１．０ｍｇ·ｋｇ－１，ｉｖ）不影响ＯＡ诱导的低血压反应，但可浓度依赖性抑制ＯＡ引起的支气管和肺内气道微血管渗漏；同时能阻断ＳＰ引起的低血压和各组织微血管渗漏反应。结论：抗原诱导的气道微血管渗漏反应与内源性速激肽有关，ＣＰ－９６３４５对此有选择性抑制作用
Objective: To investigate whether endogenous tachykinins are involved in antigen-induced cardiovascular responses in guinea pigs. Methods: The effects of tachykinin NK-1 receptor antagonist CP-96345 on blood pressure and evoked potentials of Evans blue in different tissues of guinea pigs induced by iv antigen (ovalbumin, OA) or substance P (SP) were observed. Results: OA (5 mg · kg -1) or SP (2 μg · kg -1) all caused a decrease in blood pressure in anesthetized guinea pigs; increased Evans blue exudation in the bronchi, lung airways, atria, ventricles, auricles and bladder. CP-96345 (0.3, 1.0 mg · kg-1, iv) did not affect the OA-induced hypotensive response, but inhibited the bronchial and pulmonary microvascular leakage induced by OA in a concentration-dependent manner. SP-induced hypotension and microvascular leakage in each tissue. CONCLUSIONS: Antigen-induced airway microvascular leakage is associated with endogenous tachykinins, which is selectively inhibited by CP-96345