Rinoplastia experimental com enxerto autógeno de costela em cães / Experimental rhinoplasty using autogenous rib graft in dogs

O uso de costela autógena para correção de defeito criado no osso nasal em cães foi utilizado em 15 animais, separados em três grupos de pós-operatório, em que, após 30, 60 e 90 dias, finalizavam-se seus acompanhamentos. Cada grupo era composto de quatro animais enxertados e um animal-controle, no qual se utilizava o material do próprio defeito criado para coaptação. Os animais receberam monitoração clínica diária, e a integração do enxerto foi avaliada com exames radiográficos obtidos a cada 15 dias, quando se realizou o exame histológico. A técnica cirúrgica foi de fácil execução e possui praticidade em seu uso e foi suficiente para a correção de todos os defeitos criados. O efeito estético foi satisfatório, os exames radiográficos comprovaram a integração do enxerto, e a avaliação histológica evidenciou a presença de células compatíveis com a viabilização da técnica proposta.

The use of autologous rib to correct an experimental nasal bone lesion in dogs was performed in 15 animals, distributed in three post-operatory groups, and after 30, 60, and 90 days their clinical monitoring were finished. Each group was composed of four grafted animals and a control, in which it was used the material collected from the defect for coaptation. The animals received daily clinical monitoring and the graft integration was evaluated with radiographic exams taken every 15 days when the histological exam was performed. The surgical technique was easy to perform and had practical use. It was sufficient to correct all created lesions. The aesthetical effect was satisfactory; the radiographic exams proved the graft integration and the histological evaluation showed the presence of cells compatible with the viability of the technique.

Effect of the L- or D-aspartate on ecto-5'nucleotidase activity and on cellular viability in cultured neurons: participation of the adenosine A(2A) receptors.

Glutamate increases the extracellular adenosine levels, an important endogenous neuromodulator. The neurotoxicity induced by glutamate increases the ecto-5'-nucleotidase activity in neurons, which produces adenosine from AMP. L- and D-aspartate (Asp) mimic most of the actions of glutamate in the N-methyl-D-aspartate (NMDA) receptors. In the present study, both amino acids stimulated the ecto-5'-nucleotidase activity in cerebellar granule cells. MK-801 and AP-5 prevented the L- and D-Asp-evoked activation of ecto-5'-nucleotidase. Both NMDA receptor antagonists prevented completely the damage induced by L-Asp, but partially the D-Asp-induced damage. The antagonist of adenosine A(2A) receptors (ZM 241385) prevented totally the L- Asp-induced cellular death, but partially the neurotoxicity induced by D-Asp and the antagonist of adenosine A(1) receptors (CPT) had no effect. The results indicated a different involvement of NMDA receptors on the L- or D-Asp-evoked activation of ecto-5'-nucleotidase and on cellular damage. The adenosine formed from ecto-5'-nucleotidase stimulation preferentially acted on adenosine A(2A) receptor which is probably co-operating with the neurotoxicity induced by amino acids.