xidativo dos neutrófilos de ovinos tratados com monensina sódica e experimentalmente submetidos com monensina sódica e experimentalmente submetidos com monensina sódica e experimentalmente submetidos com monensina sódica e experimentalmente submetidos com monensina sódica e experimentalmente submetidos
2002
.. ..- Afonso J.A.B., Ciarlini P.C., Kuchembuck M.R.G., Kohayagawa A., Feltrin L.P.Z., Ciarlini L.D.R.P., Laposy C.B., Mendonca C.L. & Takahira R.K. 2002. [Oxidative metabolism of the Oxidative metabolism of the Oxidative metabolism of the Oxidative metabolism of the Oxidative metabolism of the neutrophils in sheep treated with sodium monensin and experimentally submitted to neutrophils in sheep treated with sodium monensin and experimentally submitted to neutrophils in sheep treated with sodium monensin and experimentally submitted to neutrophils in sheep treated with sodium monensin and experimentally submitted to neutrophils in sheep treated with sodium monensin and experimentally submitted to ruminal acidosis. ruminal acidosis. ruminal acidosis. ruminal acidosis. ruminal acidosis.] Metabolismo oxidativo dos neutrofilos de ovinos tratados com monensina sodica e experimentalmente submetidos a acidose ruminal. Pesquisa Veterinaria Brasileira 22(4):129134. Clinica de Bovinos, UFRPE, Cx. Postal 152, Garanhuns, PE 55292-901, Brazil. Ruminal acidosis is due to excessive ingestion of carbohydrates of rapid fermentation without previous adaptation of the microorganisms, causing severe metabolic disturbances to the animals. The objective of the present study was to assess the neutrophilic oxidative metabolism in sheep treated with sodium monensin in experimentally induced ruminal lactic acidosis. A total of 18 male sheep, half-bred (Ideal x Merino), fistulated in the rumen, were used; nine of them received 33 mg/kg of the ionophore diet per day, for 30 days; the others were controls. The acidosis was induced by supplying 15g of sucrose/kg of body weight. The clinical evaluation and the rumen and blood samples were obtained before (0h) and at 6, 12, 24 and 48 hours post-induction. In both groups, all the animals presented clinical manifestations of ruminal lactic acidosis 6 hours after the induction. From this period on, a significant pH decrease (P<0.05) was observed in the ruminal fluid, which reached levels below 5. There were relevant differences (P<0.05) between the groups 12 hours after the induction, when the sheep treated with monensin had higher values than those of the control group. During this period, the oxidative metabolism of the neutrophils remained inhibited, and the reestablishment of this function only occurred in the sheep which received monensin. Blood pH, plasmatic glucose and the ionizable calcium suffered alterations within its levels. The seric cortisol concentration rose significantly (P<0.05) in both groups, although differences (P<0.05) between them were found at the end of the observation period. The treatment with monensin did not influence the oxidative metabolism of the neutrophils inhibited by the lactic acidosis; however, a faster recovery of this metabolism was verified in the animals treated with the ionophore.
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