Resposta em parâmetros sanguíneos e urinários de vacas leiteiras ao aumento no balanço cátion-aniônico da dieta

Estudou-se efeito de quatro níveis de dietas catiônicas sobre os parâmetros ácido-base do sangue e o pH urinário de vacas em lactação. Para a manipulação dos níveis do balanço cátion-amônico da dieta (BCAD), foram adicionadas diferentes concentrações de bicarbonato de sódio às dietas, obtendo-se os seguintes tratamentos: +150, +250, +400 e +500mEq/kg de matéria seca. O experimento foi realizado durante o verão, por um período total de 72 dias, utilizando-se oito vacas da raça Holandesa após o pico de lactação, distribuídas em quadrado latino (4x4), replicado, em que cada período teve duração de 18 dias. O pH urinário e o bicarbonato, o pH, o CO2 total e a pCO2 do sangue aumentaram linearmente (P<0,01) com o aumento do BCAD. As concentrações de sódio e potássio do sangue não foram modificadas (P>0,05) pelo BCAD. A concentração de cloro no sangue diminuiu linearmente (P<0,01) com o aumento do BCAD. O aumento do BCAD afetou o equilíbrio ácido-base das vacas, promovendo efeito alcalinogênico, o que poderia levar a diferenças significativas no desempenho do animal.

Cyclic nitroxides inhibit the toxicity of nitric oxide-derived oxidants: mechanisms and implications

The substantial therapeutic potential of tempol (4-hydroxy-2,2,6,6-tetramethyl-1-piperidinyloxy) and related cyclic nitroxides as antioxidants has stimulated innumerous studies of their reactions with reactive oxygen species. In comparison, reactions of nitroxides with nitric oxide-derived oxidants have been less frequently investigated. Nevertheless, this is relevant because tempol has also been shown to protect animals from injuries associated with inflammatory conditions, which are characterized by the increased production of nitric oxide and its derived oxidants. Here, we review recent studies addressing the mechanisms by which cyclic nitroxides attenuate the toxicity of nitric oxidederived oxidants. As an example, we present data showing that tempol protects mice from acetaminophen-induced hepatotoxicity and discuss the possible protection mechanism. In view of the summarized studies, it is proposed that nitroxides attenuate tissue injury under inflammatory conditions mainly because of their ability to react rapidly with nitrogen dioxide and carbonate radical. In the process the nitroxides are oxidized to the corresponding oxammonium cation, which, in turn, can be recycled back to the nitroxides by reacting with upstream species, such as peroxynitrite and hydrogen peroxide, or with cellular reductants. An auxiliary protection mechanism may be down-regulation of inducible nitric oxide synthase expression. The possible therapeutic implications of these mechanisms are addressed.