Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
6285484 | Neuroscience Letters | 2009 | 6 Pages |
Abstract
In a previous study, we concluded that overproduction of nitric oxide (NO) by inducible nitric oxide synthase (iNOS) in the late phase of sepsis prevents hypothalamic activation, blunts vasopressin secretion and contributes to hypotension, irreversible shock and death. The aim of this follow-up study was to evaluate if the same neuronal activation pattern happens in brain structures related to cardiovascular functions. Male Wistar rats received intraperitoneal injections of aminoguanidine, an iNOS inhibitor, or saline 30Â min before cecal ligation and puncture (CLP) or sham surgeries. The animals were perfused 6 or 24Â h after the surgeries and the brains were removed and processed for Fos immunocytochemistry. We observed an increase (PÂ <Â 0.001) in c-fos expression 6Â h after CLP in the area postrema (AP), nucleus of the tractus solitarius (NTS), ventral lateral medulla (VLM), locus coeruleus (LC) and parabrachial nucleus (PB). At 24Â h after CLP, however, c-fos expression was strongly decreased in all these nuclei (PÂ <Â 0.05), except for the VLM. Aminoguanidine reduced c-fos expression in the AP and NTS at 6Â h after CLP, but showed an opposite effect at 24Â h, with an increase in the AP, NTS, and also in the VLM. No such effect was observed in the LC and PB at 6 or 24Â h. In all control animals, c-fos expression was minimal or absent. We conclude that in the early phase of sepsis iNOS-derived NO may be partially responsible for the activation of brain structures related to cardiovascular regulation. During the late phase, however, this activation is reduced or abolished.
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Authors
Fernando Henrique Pascoti Bruhn, Pollyanna Barbosa Farias Corrêa, Gabriela Ravanelli Oliveira-Pelegrin, Maria José Alves Rocha,