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Showing 141 to 146 of 146 (0.033 seconds)Spelling suggestions: "subject:"bicarbonate."" "subject:"dicarbonate.""
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<i>Helicobacter pylori</i> and Gastric Protection Mechanisms : An <i>in vivo</i> Study in Mice and RatsHenriksnäs, Johanna January 2005 (has links)
<p>The stomach is frequently exposed to hazardous agents and to resist this harsh environment, several protective mechanisms exist. Of special interest is the gastric pathogen <i>Helicobacter pylori </i>which causes gastritis, ulcers and cancer but the mechanism leading to these diseases are still unclear. However it is very likely that <i>H. pylori </i>negatively influence the protection mechanisms that exist in the stomach. </p><p>The aims of the present investigation were first to develop an in vivo mouse model in which different protection mechanisms could be studied, and second to investigate the influence of <i>H. pylori</i> on these mechanisms. </p><p>An in vivo preparation of the gastric mucosa in mice was developed. This preparation allows studies of different gastric mucosal variables and can also be applied for studies in other gastro-intestinal organs. </p><p>Mice chronically infected with <i>H. pylori</i>, were shown to have a reduced ability of the mucosa to maintain a neutral pH at the epithelial cell surface. This could be due to the thinner inner, firmly adherent mucus gel layer, and/or to defective bicarbonate transport across the epithelium. The Cl<sup>-</sup>/HCO<sub>3</sub><sup>-</sup> exchanger SLC26A9 was inhibited by NH<sub>4</sub><sup>+</sup>, which also is produced by <i>H. pylori</i>. The mRNA levels of SLC26A9 were upregulated in infected mice, suggesting a way to overcome the inhibition of the transporter. Furthermore, the hyperemic response to acid pH 2 and 1.5 was abolished in these mice. The mechanisms by which the bacteria could alter the blood flow response might involve inhibition of the epithelial iNOS.</p><p>Water extracts of <i>H. pylori </i>(HPE) reduces the blood flow acutely through an iNOS and nerve-mediated pathway, possibly through the endogenous iNOS inhibitor ADMA. Furthermore, HPE alters the blood flow response to acid as the hyperemic response to acid pH 0.8 is accentuated in mice treated with HPE. </p>
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Helicobacter pylori and Gastric Protection Mechanisms : An in vivo Study in Mice and RatsHenriksnäs, Johanna January 2005 (has links)
The stomach is frequently exposed to hazardous agents and to resist this harsh environment, several protective mechanisms exist. Of special interest is the gastric pathogen Helicobacter pylori which causes gastritis, ulcers and cancer but the mechanism leading to these diseases are still unclear. However it is very likely that H. pylori negatively influence the protection mechanisms that exist in the stomach. The aims of the present investigation were first to develop an in vivo mouse model in which different protection mechanisms could be studied, and second to investigate the influence of H. pylori on these mechanisms. An in vivo preparation of the gastric mucosa in mice was developed. This preparation allows studies of different gastric mucosal variables and can also be applied for studies in other gastro-intestinal organs. Mice chronically infected with H. pylori, were shown to have a reduced ability of the mucosa to maintain a neutral pH at the epithelial cell surface. This could be due to the thinner inner, firmly adherent mucus gel layer, and/or to defective bicarbonate transport across the epithelium. The Cl-/HCO3- exchanger SLC26A9 was inhibited by NH4+, which also is produced by H. pylori. The mRNA levels of SLC26A9 were upregulated in infected mice, suggesting a way to overcome the inhibition of the transporter. Furthermore, the hyperemic response to acid pH 2 and 1.5 was abolished in these mice. The mechanisms by which the bacteria could alter the blood flow response might involve inhibition of the epithelial iNOS. Water extracts of H. pylori (HPE) reduces the blood flow acutely through an iNOS and nerve-mediated pathway, possibly through the endogenous iNOS inhibitor ADMA. Furthermore, HPE alters the blood flow response to acid as the hyperemic response to acid pH 0.8 is accentuated in mice treated with HPE.
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Fyllnadsnivåers påverkan, tidsförlängning innan analys och blodprovers stabilitet / The Impact of Lower Sample Volumes, Pre-analytical Delay and Blood Sample StabilityChahrour, Yasmin, Ishak, Helen January 2018 (has links)
Bakgrund: Provmaterial för joniserat kalcium är känsligt för pH-förändringar och med tanke på svårstuckna patienter är det betydelsefullt att undersöka lägre fyllnadsnivåers påverkan på analysresultatet. På grund av olika pre-analytiska faktorer kan tidsgränsen (4 timmar) för analys av standardbikarbonat överskridas. Förvaring av post-analytiska serumprover medför att kompletteringsanalyser kan beställas. Begränsad dokumentation finns om avkorkade serumprovers stabilitet i rumstemperatur. Syfte: Syftet var att undersöka hur lägre fyllnadsnivåer av serum påverkar analysresultatet för joniserat kalcium, om standardbikarbonatsprover på helblod kan analyseras senare än 4 timmar och hur länge serumprover kan stå i rumstemperatur utan kork för eventuella kompletteringsanalyser. Metod: Koncentrationen av analyten joniserat kalcium i serumprover med fyllnadsnivåerna 1 mL och 2 mL jämfördes med maximalt fyllda provrör. Kylskåpsförvarade helblodsprover analyserades för standardbikarbonat efter 4-7 timmar. Avkorkade serumprover analyserades för 10 biokemiska analyter efter att ha stått i rumstemperatur 2-8 timmar. Genomsnittlig procentuell avvikelse jämfördes med en analytisk och biologisk imprecisionsgräns för att bedöma analyters stabilitet. Resultat och slutsatser: Analysresultat av joniserat kalcium i lägre fyllnadsnivåer var tillförlitliga. Stabiliteten av standardbikarbonatsproverna kunde inte bedömas och därmed kunde inte en eventuell tidsgränsändring rekommenderas. De biokemiska analyterna var stabila upp till 8 timmar i rumstemperatur. / Background: Ionized calcium concentrations decrease when samples are exposed to air. Due to pre-analytical factors, the 4 hour time limit for analysis of standard bicarbonate, can sometimes be exceeded. There is limited documentation about additional analyses on post-analytic decapped serum samples stored at room temperature. Aim: The aim was to examine how lower sample volumes affect the concentration of ionized calcium, if the time limit for analysis of standard bicarbonate on whole blood can be prolonged and how long decapped serum samples can be stored at room temperature for eventual additional analyses. Methods: The concentration of ionized calcium was analyzed on serum samples filled with 1 mL and 2 mL and were compared to maximally filled samples. Refrigerated whole blood samples were analyzed for standard bicarbonate after 4-7 hours. Ten biochemical analytes were measured in decapped serum samples after 2-8 hours of storage at room temperature. The mean percentage deviation was compared to an analytical and biological imprecision limit to determine analyte stability. Results and conclusions: Ionized calcium concentrations in lower sample volumes were reliable. The stability of standard bicarbonate could not be determined, therefore a longer possible time limit could not be recommended. The biochemical analytes were stable for 8 hours.
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Associação entre carga ácida da dieta e bicarbonato sérico em portadores de doença renal crônica / Association between dietary acid load and serum bicarbonate in patients with chronic kidney diseaseLarissa Rodrigues Neto Angeloco 15 December 2017 (has links)
A acidose metabólica é um achado comum em pacientes portadores de Doença Renal Crônica (DRC). Acredita-se que a dieta pode afetar o equilíbrio ácidobase do corpo por meio do fornecimento de precursores ácidos ou de base. No entanto, os resultados inconclusivos apontados na literatura indicam que ainda são necessários estudos bem delineados para comprovar a existência dessa associação. O principal objetivo desse estudo foi determinar o potencial de carga ácida renal (PRAL) proveniente da dieta e avaliar a sua associação com o bicarbonato sérico (HCO3) em pacientes com DRC enquanto em suas dietas habituais. Associações do HCO3 com o gasto energético de repouso (GER) e com oxidações proteicas e lipícas também foram estudadas. Trata-se de um estudo transversal realizado com 100 pacientes distribuídos igualmente nos estágios 3 e 4 da DRC entre 20 e 69 anos. Avaliação do estado nutricional foi feita por meio da antropometria, registro alimentar e exames bioquímicos, o qual incluiu os produtos proteicos de oxidação avançada e os isoprostanos. O HCO3 foi determinado por meio da gasometria venosa. GER foi medido pela calorimetria indireta. O PRAL foi determinado por meio do registro alimentar usando um algoritmo que inclui dados dietéticos da ingestão de proteína, fósforo, magnésio, cálcio e potássio descritos por Remer e Manz (1995). Também foi feita a diferenciação no consumo de proteína animal e vegetal. A análise dos resultados foi feita em quartis de HCO3 para as variáveis GER e parâmetros de oxidação, o restante das análises foram feitas por quartis de PRAL. Para comparação das variações médias dos quartis foi utilizado o teste one-way ANOVA. A associação entre a estimativa do PRAL e o HCO3 foi avaliada por modelos de regressão linear ajustados. A maior parte dos nossos pacientes portadores de DRC encontravam-se com excesso de peso associado a um aumento da circunferência abdominal e da porcentagem de gordura corporal. A mediana do PRAL foi de 6,8 mEq/dia com uma variação entre -24 a 52 mEq/dia. O PRAL mais elevado foi associado com o HCO3 mais baixo de uma forma graduada (p < 0.02). Encontramos uma diferença de 2,07 mmol/L no HCO3 entre o primeiro e o último quartil, sendo o valor do último quartil de PRAL menor em relação ao primeiro. A proteína animal apresentou uma correlação inversa com o bicarbonato sérico. O GER e os marcadores de oxidação lipíca e proteica não apresentaram associações com os níveis de HCO3. Esses resultados reforçam a possibilidade de que dietas com alto teor de carga ácida podem desempenhar um papel relevante no equilíbrio ácidobase em pacientes portadores de DRC, além de consolidar o uso da carga ácida da dieta como uma abordagem diferencial e complementar às outras estratégias no tratamento dietético da DRC. / Metabolic acidosis is a common complication in patients with chronic kidney disease (CKD). Acid-inducing diets are believed to impact on acid-base balance. However, well-designed studies are still needed to prove the association between dietary acid load and serum bicarbonate. The main aim of this study was to calculate the potential renal acid load (PRAL) of selected, frequently consumed foods and to evaluate its association with serum bicarbonate (HCO3) in patients with CKD. Associations of HCO3 with resting energy expenditure (REE) and with protein and lipid oxidation were also studied. It is a cross-sectional study with 100 patients equally distributed in stages 3 and 4 of CKD between 20 and 69 years. Nutritional status was assessed by anthropometric measurements, 3-day food recall, biochemical analysis including advanced oxidation protein products and isoprostanes. Venous blood gases was used to measure HCO3. GER was measured by indirect calorimetry. PRAL was determined by food record using an algorithm that includes protein, phosphorus, magnesium, calcium and potassium intake described by Remer and Manz (1995). Dietary intake of animal and vegetable protein were also evaluate. For analysis, we used quartiles of HCO3 for GER and oxidation parameters and for the others variables we used quartilhes of PRAL. ANOVA one-way test was used to compare the mean of the quartiles. The association between PRAL and HCO3 was assessed by linear regression models. Most of the patients were overweight with increased waist circumference and body fat. The median PRAL was 6.8 mEq/day with a variation between -24 to 52 mEq/day. Higher PRAL was associated with lower serum bicarbonate in a graded fashion (P trend 0.02). Serum bicarbonate was 2.07 mEq/L lower among those in the highest compared with the lowest quartile of PRAL. Animal protein was inversely correlated with serum bicarbonate. REE and lipid and protein oxidation markers showed no association with HCO3 levels. These results reinforce the possibility that diets with high dietary acid load may play a relevant role in the acid-base balance in CKD patients. In addition to consolidating the use of PRAL as a differential and complementary approach to other strategies in the nutritional treatment of CKD.
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Third Place Winner of the Conrad Jobst Award in the Gold Medal Paper Competition. Prevention of Spinal Cord Dysfunction in a New Model of Spinal Cord IschemiaLopez, S, Manahan, E, Evans, J. R., Kao, R. L., Browder, W. 01 January 1995 (has links)
Paraplegia or paraparesis caused by temporary cross-clamping of the aorta is a devastating sequela in patients after surgery of the thoracoabdominal aorta. No effective clinical method is available to protect the spinal cord from ischemic reperfusion injury. A small animal (rat) model of spinal cord ischemia is established to better understand the pathophysiological events and to evaluate potential treatments. Eighty-one male Sprague-Dawley rats weighing 300 g to 350 g were used for model development (45) and treatment evaluation (36). The heparinized and anesthetized rat was supported by a respirator following tracheostomy. The thoracic aorta was cannulated via the left carotid artery for post-clamping intra-aortic treatment solution administration. After thoracotomy, the aorta was freed and temporarily clamped just distal to the left subclavian artery and just proximal to the diaphragm for different time intervals: 0, 5, 10, 15, 20, 25, 30, 35, and 40 minutes (five animals per group). The motor function of the lower extremities postoperatively showed consistent impairment after 30 minutes clamping (5/5 rats were paralyzed), and this time interval was used for treatment evaluation. For each treatment, six animals per group were used, and direct local intra-aortic infusion of physiologic solution (2 mL) at different temperatures with or without buffer substances was given immediately after double cross-clamp to protect the ischemic spinal cord. Arterial blood (2 mL) was infused in the control group. The data indicate that the addition of HCO3-(20 mM) to the hypothermic (15 degrees C) solution offered complete protection of the spinal cord from ischemic injury.(ABSTRACT TRUNCATED AT 250 WORDS)
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Das Auftreten acidophiler/calcifuger Pflanzenarten in Kalk-Halbtrockenrasen / The occurence of acidophile/calcifuge plant species in semi-arid calcareous grasslandsFühner, Christoph 02 November 2005 (has links)
No description available.
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