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Tytuł oryginału: Gastric hyperemic response induced bay acid back-diffusion in rat stomachs following barrier disruption - relation to vanilloid type-1 receptors.
Autorzy: Tashima Kimihito, Nakashima Masato, Kagawa Shigeru, Kato Shinichi, Takeuchi Koji
Źródło: Med. Sci. Monitor 2002: 8 (5) s.BR157-BR163, il., bibliogr. 20 poz.
Sygnatura GBL: 313,278

Hasła klasyfikacyjne GBL:
  • farmacja
  • gastroenterologia

    Typ dokumentu:
  • praca doświadczalna
  • tytuł obcojęzyczny

    Wskaźnik treści:
  • zwierzęta
  • szczury
  • płeć męska

    Streszczenie angielskie: Acid back-diffusion activates capsaicin-sensitive sensory neurons (CSN), leading to gastric hyperemic response. We examined the role of vanilloid type-1 receptor (VR1) in gastric hyperemic and ulcerogenic responses in rat stomach following exposure to taurocholate (TC). Under urethane anesthesia, a rat stomach was mounted on an ex-vivo chamber, perfused with 50 mM HCl, and changes in PD, gastric mucosal blood flow (GMBF), and luminal acid loss were measured before and after exposure to 20 mM TC for 30 min, in presence of omeprazole. Capsazepine was co-applied with TC for 30 min to the stomach, while ruthenium red was given i.v. 10 min before TC treatment. TC caused a marked PD reduction, followed by an increase of acid loss and GMBF, resultin in minimal damage in the mucosa. Chemical ablation of CSN attenuated the GMBF response to TC without affecting PD reduction and acid loss, and resulted in severe lesions, while none of these responses induced by TC was significantly affected by either capsazepine or ruthenium red. Intragastric capsaicin increased GMBF, and this response was attenuated by both capsazepine and ruthenium red as well as sensory deafferentation. Both acid back-diffusion and capsaicin increase GMBF mediated by CSN, yet their modes of action differ in terms of capsazepine- or ruthenium red-sensitvity. Although the luminal H+ plays a modulator role for the physiological response mediated by CSN in the stomach, it is unlikely that the action results from the interaction of H+ with the capsazepine- or ruthenium red-sensitive site of VR1.

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