Participação de fibras sensoriais na resposta edematogenica induzida pela enterotoxina estafilococica do tipo B em camundongos

AUTOR(ES)
DATA DE PUBLICAÇÃO

1999

RESUMO

In this study, we investigated the participation of sensory fibers in the mouse paw oedema induced by staphylococcãI enterotoxin type B (SEB; 25 Ilg/paw). The NK1 receptor antagonist SR140333 (120 nmolJkg, s.c. + 120 nmolJkg, i.v.) significantly inhibited the plasma protein extravasation and oedema formation induced by SEB (37 and 35%, respectively). The oedema and exsudation induced by the NK1 receptor agonist (GR73632; 50 pmol/paw) were also reduced significantly by SR140333 (40 and 88%, respectively). The oedematogenic activity of the NK2 receptor antagonist SR48968 (1.7 J.l11lolJKg, i.v.) did not affect SEB or GR73632. In addition, the oedema and plasma exsudation-induced by SEB were not altered by the vasodilator CGRP (100 and 300 pmol/paw). However, GR73632-induced oedema (50 pmol/paw) was significantly increased by CGRP. Pretreating the mice with the B2 antagonist receptor (HOE 140; 400 nmolJk~, i.v.) showed a significantly reduced the SEB-induced oedema and exsudation (35 and 34%, respectively). Oedema caused by bradykinin (3 nmol/paw) was also significantly reduced by HOE 140. Simultaneol!J,s treatment with SR140333 and HOE 140 inhibited SEB-induced paw oedem~, but only to an extent similar to that observed when these antagonists were administered alone. SR140333 (120 nmolJkg, s.c. + 120 nmolJkg, i.v.) significantly reduced the oedema (62%) and exsudation (49%) induced by bradykinin. The vanilloid antagonist capsazepine (100 JlmolJKg, s.c.) significantly reduced in the oedema (53%) and exsudation (45%) induced by SEB. This antagonist (50 and 100 JlmolJkg, s.c.) also dose-dependently inhibited the paw oedema induced by capsaicin (5 Ilg/paw).

ASSUNTO(S)

inflamação toxinas bradicinina edema

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