890 resultados para Sodium Bicarbonate


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Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)

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Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)

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Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)

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In this work, differential scanning calorimetry (DSC) was used to study the mechanism of crystallization of 5OP(2)O(5-)27.8Na(2)O-16ZnO-6.2Al(2)O(3) glass. DSC measurements were performed on bulk and powdered glasses with different particle size. The curve for bulk glass shows one crystallization peak while powdered glasses presented two distinct crystallization peaks. Based on DSC studies, the activation energies obtained were 336 +/- 6 and 213 +/- 3 U mol(-1), associated with first and second crystallization peaks, respectively. Analyzing the DSC parameters as a function of particle size, the Avrami n parameter suggests that the peak at low temperature may be associated with surface crystallization while the peak at high temperature is associated with bulk crystallization. (C) 2002 Elsevier B.V. Ltd. All rights reserved.

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OBJETIVO: Avaliar as alterações histológicas e biomecânicas do diclofenaco de sódio na mucosa intestinal do rato e a associação com o uso de Imipenem. MÉTODOS: Foram estudados 240 ratos Wistar distribuídos aleatoriamente em quatro grupos experimentais: GI: 60 ratos tratados com injeção IM de soro fisiológico 0,9%; GII: 60 ratos tratados com injeção IM de diclofenaco de sódio na dose de 6mg/kg de peso por 4 dias; GIII: 60 ratos tratados com injeção IM de Imipenem na dose de 30 mg/kg de peso por 4 dias; GIV: 60 ratos tratados com injeção IM de soro fisiológico e diclofenaco de sódio nas doses acima. em cada grupo os animais foram posteriormente divididos em 4 momentos de 15 animais em cada um para sacrifício, respectivamente, no 4º, 7º, 14º e 21º dias após o início do tratamento. As alterações da cavidade abdominal, assim como as características histológicas e de força de ruptura do intestino delgado foram analisadas em cada momento, em cada grupo. RESULTADOS: Não foram encontradas alterações histológicas e biomecânicas nos animais do Grupo I nesse estudo. Lesões ulceradas na mucosa do intestino delgado foram observadas nos animais tratados com diclofenaco de sódio, assim como diminuição da força de ruptura. As lesões ulceradas encontradas foram prevenidas pelo uso de Imipenem. CONCLUSÃO: O diclofenaco de sódio induz lesões ulceradas na mucosa intestinal do rato que podem ser prevenidas pelo uso de Imipenem.

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Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)

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Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)

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Prototheca zopfii has been considered one of the most important causes of environmental mastitis in Brazil. These algae are refractory to conventional therapy and cause great damage to the mammary gland. The present study evaluated the in vitro algaecide effect of sodium hypochlorite and iodine based antiseptics on 27 P. zopfii strains isolated from the milk of cattle. Low concentrations of sodium hypochlorite (0.0390625-0.15625%) and iodine (0.15625-0.625%) were effective against the isolates. These antiseptics may be recommended for hygiene routines, pre and postdipping and cauterization of bovine mammary glands infected by P. zopfii. (C) 2009 Elsevier Ltd. All rights reserved.

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O presente estudo teve por objetivo avaliar o efeito da utilização de níveis crescentes do gluconato de sódio sobre o desempenho, o rendimento de carcaça e de partes e a morfometria da mucosa intestinal de frangos de corte de 22 a 42 dias de idade. Foram utilizados 1200 frangos de corte da linhagem Cobb, distribuídos em um delineamento inteiramente casualizado, envolvendo cinco tratamentos (0,00; 0,10; 0,20; 0,30 e 0,40% de gluconato de sódio) com oito repetições de 30 aves cada parcela. As variáveis foram submetidas à análise de variância e em caso de significância estatística foram realizadas análises de regressão pelos modelos polinomial e quadrático. A inclusão do gluconato de sódio não afetou o desempenho e o rendimento de carcaça e de partes. Entretanto, exerceu efeito benéfico sobre a morfometria da mucosa intestinal do duodeno e do jejuno.

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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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GABAergic activation in the lateral parabrachial nucleus (LPBN) induces sodium and water intake in satiated and normovolemic rats. In the present study we investigated the effects of GABA(A) receptor activation in the LPBN on 0.3 M NaCl, water, 2% sucrose and food intake in rats submitted to sodium depletion (treatment with the diuretic furosemide subcutaneously + sodium deficient food for 24 h), 24 h food deprivation or 24 h water deprivation. Male Holtzman rats with bilateral stainless steel cannulas implanted into the LPBN were used. In sodium depleted rats, muscimol (GABA(A) receptor agonist, 0.5 nmol/0.2 mu/l), bilaterally injected into the LPBN, produced an inconsistent increase of water intake and two opposite effects on 0.3 M NaCl intake: an early inhibition (4.3 +/- 2.7 versus saline: 14.4 +/- 1.0 ml/15 min) and a late facilitation (37.6 +/- 2.7 versus saline: 21.1 +/- 0.9 ml/180 min). The pretreatment of the LPBN with bicuculline (GABA(A) receptor antagonist, 1.6 nmol) abolished these effects of muscimol. Muscimol into the LPBN also reduced food deprivation-induced food intake in the first 30 min of test (1.7 +/- 0.6 g versus saline: 4.1 +/- 0.6 g), without changing water deprivation-induced water intake or 2% sucrose intake in sodium depleted rats. Therefore, although GABAA receptors in the LPBN are not tonically involved in the control of sodium depletion-induced sodium intake, GABAA receptor activation in the LPBN produces an early inhibition and a late facilitation of sodium depletion-induced sodium intake. GABAA activation in the LPBN also inhibits food intake, while it consistently increases only sodium intake and not water, food or sucrose intake. (c) 2007 Elsevier B.V. All rights reserved.

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Inhibitory mechanisms in the lateral parabrachial nucleus (LPBN) and central GABAergic mechanisms are involved in the regulation of water and NaCl intake. Besides increasing fluid depletion-induced sodium intake, the activation of GABA(A) receptors with muscimol into the LPBN also induces ingestion of 0.3 M NaCl in normonatremic, euhydrated rats. It has been suggested that inhibitory mechanisms activated by osmotic signals are blocked by GABAA receptor activation in the LPBN, thereby increasing hypertonic NaCl intake. Therefore, in the present study we investigated the effects of muscimol injected into the LPBN on water and 0.3 M NaCl intake in hyperosmotic cell-dehydrated rats (rats treated with an intragastric load of 2 M NaCl). Male Wistar rats with stainless steel cannulas implanted bilaterally into the LPBN were used. In euhydrated rats, muscimol (0.5 nmol/0.2 mu l), bilaterally injected into the LPBN, induced ingestion of 0.3 M NaCl (24.6 +/- 7.9 vs. vehicle: 0.5 +/- 0.3 ml/180 min) and water (6.3 +/- 2.1 vs. vehicle: 0.5 +/- 0.3 ml/180 min). One hour after intragastric 2 M NaCl load (2 ml), bilateral injections of muscimol into the LPBN also induced 0.3 M NaCl intake (22.1 +/- 5.2 vs. vehicle: 0.9 +/- 0.8 ml/210 min) and water intake (16.5 +/- 3.6 vs. vehicle: 7.8 +/- 1.8 ml/210 min). The GABAA antagonist bicuculline (0.4 nmol/0.2 mu l) into the LPBN reduced the effect of muscimol on 0.3 M NaCl intake (7.1 +/- 2.1 ml/210 min). Therefore, the activation of GABAA receptors in the LPBN induces ingestion of 0.3 M NaCl by hyperosmotic cell-dehydrated rats, suggesting that plasma levels of renin or osmolarity do not affect sodium intake after the blockade of LPBN inhibitory mechanisms with muscimol. (c) 2007 Elsevier B.V. All rights reserved.