Uchida Y, Tanaka K, Harada Y, Ueno A, Katori M
Inflammation. 1983 Jun;7(2):121-31. doi: 10.1007/BF00917817.
Rat pleurisy was induced by intrapleural injection of lambda-carrageenin. The pleural exudate began to be accumulated 1-3 h after carrageenin administration and showed a peak at 19 h. The levels of prekallikrein and high-molecular-weight (HMW), but not low-molecular-weight (LMW), kininogen in the pleural fluid were markedly decreased when compared with those in plasma. Prekallikrein in rat plasma was activated by incubation with carrageenin in vitro. Captopril increased the plasma exudation significantly at 1-5 h. Depletion of prekallikrein and HMW kininogen in rat plasma by preadministration of bromelain caused marked inhibition of the plasma exudation at 1-24 h. The rest of the plasma exudation after bromelain was further decreased by simultaneous pretreatment of rats with both bromelain and aspirin. These results clearly indicate that plasma prekallikrein was activated in the pleural cavity and bradykinin released was responsible for plasma exudation during the entire course of this pleurisy.
通过向大鼠胸膜腔内注射λ-角叉菜胶诱导胸膜炎。角叉菜胶给药后1 - 3小时开始出现胸膜渗出液积聚,并在19小时达到峰值。与血浆相比,胸腔积液中前激肽释放酶和高分子量(HMW)激肽原水平显著降低,但低分子量(LMW)激肽原水平无明显变化。大鼠血浆中的前激肽释放酶在体外与角叉菜胶孵育时被激活。卡托普利在1 - 5小时显著增加血浆渗出。预先给予菠萝蛋白酶使大鼠血浆中的前激肽释放酶和HMW激肽原耗竭,导致1 - 24小时血浆渗出明显受到抑制。在预先用菠萝蛋白酶处理大鼠的同时再用阿司匹林进行预处理,可使菠萝蛋白酶处理后剩余的血浆渗出进一步减少。这些结果清楚地表明,血浆前激肽释放酶在胸腔内被激活,释放的缓激肽是该胸膜炎整个过程中血浆渗出的原因。