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Brain edema bradykinin

Bradykinin promotes edema as shown in numerous models of brain injury including bacterial meningitis (Lorenzl et al., 1996), traumatic brain and spinal cord injury (Plesnila et al, 2001 Hellal et al, 2003 Ivashkova et al., 2006), and cerebral ischemia (Lehmberg et al., 2003 Groger et al., 2005 Klasner et al., 2006 Lumenta et al., 2006). [Pg.143]

Ivashkova Y, Svetnitsky A, Mayzler O, Pruneau D, Benifla M, Fuxman Y, Cohen A, Artru AA, Shapira Y (2006) Bradykinin B2 receptor antagonism with LF 18-1505T reduces brain edema and improves neurological outcome after closed head trauma in rats. J Trauma 61 879-885... [Pg.160]

Bradykinin is an endogenous inflammatory substance that increases vascular permeability and produces tissue edema. The kallikrein-kinin system is very rapidly activated following brain injury resulting in the activation of kallikrein that cleaves kininogen to produce bradykinin. The effects of bradykinin are mediated by two different receptors B1 and B2. Very low levels of B1 are found under normal conditions. In contrast, the B2 receptor is constitutively expressed in a wide variety of tissues including the brain and mediates the majority of bradykinin effects (Couture et al., 2001). [Pg.143]


See other pages where Brain edema bradykinin is mentioned: [Pg.125]    [Pg.143]    [Pg.156]    [Pg.158]    [Pg.159]    [Pg.164]    [Pg.136]    [Pg.162]    [Pg.10]    [Pg.697]   


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