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Activation of plasma kallikrein-kinin system and its significant role in pleural fluid accumulation of rat carrageenin-induced pleurisy

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Rat pleurisy was induced by intrapleural injection of λ-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 bradykihin released was responsible for plasma exudation during the entire course of this pleurisy.

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This work was supported in part by a Grant-in-Aid for the Scientific Research (467041) from the Ministry of Education, Science and Culture, Japan.

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Uchida, Y., Tanaka, K., Harada, Y. et al. Activation of plasma kallikrein-kinin system and its significant role in pleural fluid accumulation of rat carrageenin-induced pleurisy. Inflammation 7, 121–131 (1983). https://doi.org/10.1007/BF00917817

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  • Aspirin
  • Captopril
  • Pleural Fluid
  • Pleural Cavity
  • Fluid Accumulation