急性和慢性呼吸道炎症疾病激肽形成机制探讨

目的探讨急性和慢性呼吸道炎症过程中激肽的生成途径和机制。方法测定支气管肺癌伴阻塞性肺炎，慢性支气管炎和健康对照组支气管肺泡灌洗液（ＢＡＬＦ）凝胶过滤前后激肽、激肽形成酶活性（ＴＡＭＥｅａ），血浆血管舒缓素（ＰＫ）和α２巨球蛋白（α２Ｍ），并进一步鉴定ＴＡＭＥｅａ性质。结果急、慢性组ＴＡＭＥｅａ和激肽水平与健康对照组比较差异有显著性（Ｐ＜０００１，Ｐ＜０．０１），但两组间差异无显著性（Ｐ＞００５）；急性组ＰＫ和α２Ｍ与慢性组比较差异有显著性（Ｐ＜０００１）。凝胶过滤结果显示：急性组ＢＡＬＦ的ＴＡＭＥｅａ最高峰位于分子量约８０００００处，与第一个α２Ｍ峰重叠，而慢性组的最高峰位于４００００处。ＴＡＭＥｅａ抑制试验证实８０００００处的ＴＡＭＥｅａ来自于ＰＫ；而４００００处的ＴＡＭＥｅａ主要来源于组织血管舒缓素（ＴＫ）。结论急性呼吸道炎症的ＴＡＭＥｅａ主要来自血浆的ＰＫ；而慢性呼吸道炎症则以局部组织腺体分泌的ＴＫ为主。

Kinin generation in acute and chronic airway inflammation

Objective To investigate the kinin generation pathways in acute and chronic airway inflammation. Methods BALF from patients with acute, chronic airway inflammation and healthy controls were collected. Kinins, Plasma kallikrein, 2macroglobulin and toluenesulphonylarginine methyl ester esterase activity (TAMEea) in BALF were studied. Results Kinins and TAMEea values were significantly higher in the BALF of patients with acute and chronic airway inflammation than those in the controls, but there was no significant difference between acute and chronic groups; PK and 2 M values were significantly higher in the acute group than the in chronic one. Gel filtration revealed the highest TAMEea peak at about800 000 in theacute group, corresponding with the first 2 M peak, whereas at about 40 000 in chronic bronchitis . The inhibition test of the TAMEea showed that the TAMEea peak at 800 000 was mainly due to PK and the TAMEea peak at 40 000 was mainly due to TK. Conclusions The results indicated that in acute airway inflammation kinins seem to be mainly generated by PK, whereas in chronic inflammation kininogenases other than PK such as TK seem to be more important.