47 resultados para Alkalosis


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After a meal, dogfish exhibit a metabolic alkalosis in the bloodstream and a marked excretion of basic equivalents across the gills to the external seawater. We used the H+, K+-ATPase pump inhibitor omeprazole to determine whether these post-prandial alkaline tide events were linked to secretion of H+ (accompanied by Cl) in the stomach. Sharks were fitted with indwelling stomach tubes for pretreatment with omeprazole (five doses of 5mg omeprazole per kilogram over 48 h) or comparable volumes of vehicle (saline containing 2% DMSO) and for sampling of gastric chyme. Fish were then fed an involuntary meal by means of the stomach tube consisting of minced flatfish muscle (2% of body mass) suspended in saline (4% of body mass total volume). Omeprazole pretreatment delayed the post-prandial acidification of the gastric chyme, slowed the rise in Cl concentration of the chyme and altered the patterns of other ions, indicating inhibition of H+ and accompanying Clsecretion. Omeprazole also greatly attenuated the rise in arterial pH and bicarbonate concentrations and reduced the net excretion of basic equivalents to the water by 56% over 48h. Arterial blood CO2 pressure and plasma ions were not substantially altered. These results indicate that elevated gastric H+ secretion (as HCl) in the digestive process is the major cause of the systemic metabolic alkalosis and the accompanying rise in base excretion across the gills that constitute the alkaline tide in the dogfish.

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Purpose: The aim of this study was to determine the effect and reliability of acute and chronic sodium bicarbonate ingestion for 2000-m rowing ergometer performance (watts) and blood bicarbonate concentration [HCO3 -]. Methods: In a crossover study, 7 well-trained rowers performed paired 2000-m rowing ergometer trials under 3 double-blinded conditions: (1) 0.3 grams per kilogram of body mass (g/kg BM) acute bicarbonate; (2) 0.5 g/ kg BM daily chronic bicarbonate for 3 d; and (3) calcium carbonate placebo, in semi-counterbalanced order. For 2000-m performance and [HCO3 -], we examined differences in effects between conditions via pairwise comparisons, with differences interpreted in relation to the likelihood of exceeding smallest worthwhile change thresholds for each variable. We also calculated the within-subject variation (percent typical error). Results: There were only trivial differences in 2000-m performance between placebo (277 ± 60 W), acute bicarbonate (280 ± 65 W) and chronic bicarbonate (282 ± 65 W); however, [HCO3 -] was substantially greater after acute bicarbonate, than with chronic loading and placebo. Typical error for 2000-m mean power was 2.1% (90% confidence interval 1.4 to 4.0%) for acute bicarbonate, 3.6% (2.5 to 7.0%) for chronic bicarbonate, and 1.6% (1.1 to 3.0%) for placebo. Postsupplementation [HCO3 -] typical error was 7.3% (5.0 to 14.5%) for acute bicarbonate, 2.9% (2.0 to 5.7%) for chronic bicarbonate and 6.0% (1.4 to 11.9%) for placebo. Conclusion: Performance in 2000-m rowing ergometer trials may not substantially improve after acute or chronic bicarbonate loading. However, performances will be reliable with both acute and chronic bicarbonate loading protocols. ABSTRACT FROM AUTHOR

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Context: Sodium bicarbonate (NaHCO3) is often ingested at a dose of 0.3 g/kg body mass (BM), but ingestion protocols are inconsistent in terms of using solution or capsules, ingestion period, combining NaHCO3 with sodium citrate (Na3C6H5O7), and coingested food and fluid. Purpose: To quantify the effect of ingesting 0.3 g/ kg NaHCO3 on blood pH, [HCO3 -], and gastrointestinal (GI) symptoms over the subsequent 3 hr using a range of ingestion protocols and, thus, to determine an optimal protocol. Methods: In a crossover design, 13 physically active subjects undertook 8 NaHCO3 experimental ingestion protocols and 1 placebo protocol. Capillary blood was taken every 30 min and analyzed for pH and [HCO3 -]. GI symptoms were quantified every 30 min via questionnaire. Statistics used were pairwise comparisons between protocols; differences were interpreted in relation to smallest worthwhile changes for each variable. A likelihood of >75% was a substantial change. Results: [HCO3 -] and pH were substantially greater than in placebo for all other ingestion protocols at almost all time points. When NaHCO3 was coingested with food, the greatest [HCO3 -] (30.9 mmol/kg) and pH (7.49) and lowest incidence of GI symptoms were observed. The greatest incidence of GI side effects was observed 90 min after ingestion of 0.3 g/kg NaHCO3 solution. Conclusions: The changes in pH and [HCO3 -] for the 8 NaHCO3-ingestion protocols were similar, so an optimal protocol cannot be recommended. However, the results suggest that NaHCO3 coingested with a high-carbohydrate meal should be taken 120-150 min before exercise to induce substantial blood alkalosis and reduce GI symptoms. ABSTRACT FROM AUTHOR

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

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Estudaram-se as alterações nos eletrólitos, nos gases sanguíneos, na osmolalidade, no hematócrito, na hemoglobina, nas bases tituláveis e no anion gap no sangue venoso de 11 equinos da raça Puro Sangue Árabe, destreinados, submetidos a exercício máximo e submáximo em esteira rolante. Esses animais passaram por período de três dias de adaptação à esteira rolante e posteriormente realizaram dois exercícios testes, um de curta e outro de longa duração. Foram coletadas amostras de sangue venoso antes, imediatamente após e 30 minutos após o término dos exercícios. Após a realização do exercício máximo, observou-se diminuição significativa no pHv, na PvCO2, no HCO3, na cBase além de elevação no AG. Detectou-se também aumento do K+, do Ht e da Hb. Ao final do exercício submáximo, constatou-se somente aumento significativo no pHv, na cBase, na SatvO2 e na PvO2. Conclui-se que os equinos submetidos a exercício máximo desenvolveram acidose metabólica e alcalose respiratória compensatória, hipercalemia e aumento nos valores de hematócrito e hemoglobina. No exercício submáximo, os animais apresentaram alcalose metabólica hipoclorêmica e não ocorreram alterações no equilíbrio hidroeletrolítico.

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The increased metabolic rate during digestion is associated with changes in arterial acid-base parameters that are caused by gastric acid secretion (the 'alkaline tide'). Net transfer of HCl to the stomach lumen causes an increase in plasma HCO3- levels, but arterial pH does not change because of a ventilatory compensation that counters the metabolic alkalosis. It seems, therefore, that ventilation is controlled to preserve pH and not P-CO2, during the postprandial period. To investigate this possibility, we determined arterial acid-base parameters and the metabolic response to digestion in the snake Boa constrictor, where gastric acid secretion was inhibited pharmacologically by oral administration of omeprazole. The increase in oxygen consumption of omeprazole-treated snakes after ingestion of 30% of their own body mass was quantitatively similar to the response in untreated snakes, although the peak of the metabolic response occurred later (36 h versus 24 h). Untreated control animals exhibited a large increase in arterial plasma HCO3- concentration of approximately 12 mmol 1(-1), but arterial pH only increased by 0.12 pH units because of a simultaneous increase in arterial P-CO2 by about 10 mmHg. Omeprazole virtually abolished the changes in arterial pH and plasma HCO3- concentration during digestion and there was no increase in arterial P-CO2. The increased arterial P-CO2 during digestion is not caused, therefore, by the increased metabolism during digestion or a lower ventilatory responsiveness to ventilatory stimuli during a presumably relaxed state in digestion. Furthermore, the constant arterial P-CO2, in the absence of an alkaline tide, of omeprazole-treated snakes strongly suggests that pH rather than P-CO2 normally affects chemoreceptor activity and ventilatory drive.

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Digestion affects acid-base status, because the net transfer of HCl from the blood to the stomach lumen leads to an increase in HCO3- levels in both extra- and intracellular compartments. The increase in plasma [HCO3-], the alkaline tide, is particularly pronounced in amphibians and reptiles, but is not associated with an increased arterial pH, because of a concomitant rise in arterial Pco(2) caused by a relative hypoventilation. In this study, we investigate whether the postprandial increase in Paco(2) of the toad Bufo marinus represents a compensatory response to the increased plasma [HCO3-] or a state-dependent change in the control of pulmonary ventilation. To this end, we successfully prevented the alkaline tide, by inhibiting gastric acid secretion with omeprazole, and compared the response to that of untreated toads determined in our laboratory during the same period. In addition, we used vascular infusions of bicarbonate to mimic the alkaline tide in fasting animals. Omeprazole did not affect blood gases, acid-base and haematological parameters in fasting toads, but abolished the postprandial increase in plasma [HCO3-] and the rise in arterial Pco(2) that normally peaks 48 h into the digestive period. Vascular infusion of HCO3-, that mimicked the postprandial rise in plasma [HCO3-], led to a progressive respiratory compensation of arterial pH through increased arterial Pco(2) Thus, irrespective of whether the metabolic alkalosis is caused by gastric acid secretion in response to a meal or experimental infusion of bicarbonate, arterial pH is being maintained by an increased arterial Pco(2). It seems, therefore, that the elevated Pco(2), occuring during the postprandial period, constitutes of a regulated response to maintain pH rather than a state-dependent change in ventilatory control. (C) 2003 Elsevier B.V. All rights reserved.

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Digestion is associated with gastric secretion that leads to an alkalinisation of the blood, termed the alkaline tide. Numerous studies on different reptiles and amphibians show that while plasma bicarbonate concentration ([HCO3-](pl)) increases substantially during digestion, arterial pH (pHa) remains virtually unchanged, due to a concurrent rise in arterial PCO2 (PaCO2) caused by a relative hypoventilation. This has led to the suggestion that postprandial amphibians and reptiles regulate pHa rather than PaCO2.Here we characterize blood gases in the South American rattlesnake (Crotalus durissus) during digestion and following systemic infusions of NaHCO3 and HCl in fasting animals to induce a metabolic alkalosis or acidosis in fasting animals. The magnitude of these acid-base disturbances were similar in magnitude to that mediated by digestion and exercise. Plasma [HCOT] increased from 18.4+/-1.5 to 23.7+/-1.0 mmol L-1 during digestion and was accompanied by a respiratory compensation where PaCO2 increased from 13.0+/-0.7 to 19.1+/-1.4 mm Hg at 24 h. As a result, pHa decreased slightly, but were significantly below fasting levels 36 h into digestion. Infusion of NaHCO3 (7 mmol kg(-1)) resulted in a 10 mmol L-1 increase in plasma [HCO3-] within 1 h and was accompanied by a rapid elevation of pHa (from 7.58+/-0.01 to 7.78+/-0.02). PaCO2, however, did not change following HCO3- infusion, which indicates a lack of respiratory compensation. Following infusion of HCl (4 mmol kg(-1)), plasma pHa decreased by 0.07 units and [HCO3-](pl) was reduced by 4.6 mmol L-1 within the first 3 h. PaCO2, however, was not affected and there was no evidence for respiratory compensation.Our data show that digesting rattlesnakes exhibit respiratory compensations to the alkaline tide, whereas artificially induced metabolic acid-base disturbances of same magnitude remain uncompensated. It seems difficult to envision that the central and peripheral chemoreceptors would experience different stimuli during these conditions. One explanation for the different ventilatory responses could be that digestion induces a more relaxed state with low responsiveness to ventilatory stimuli. (C) 2005 Elsevier B.V. All rights reserved.

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Water, compared with plasma at a pH of 7.4, is a weak acid. The addition of free water to a patient should have an acidifying effect (dilutional acidosis) and the removal of it, an alkalinizing effect (concentrational alkalosis). The specific effects of free water loss or gain in a relatively complex fluid such as plasma has, to the authors' knowledge, not been reported. This information would be useful in the interpretation of the effect of changes in free water in patients. Plasma samples from goats were either evaporated in a tonometer to 80% of baseline volume or hydrated by the addition of distilled water to 120% of baseline volume. The pH and partial pressure of carbon dioxide, sodium, potassium, ionized calcium, chloride, lactate, phosphorous, albumin, and total protein concentrations were measured. Actual base excess (ABE), standard bicarbonate, anion gap, strong ion difference, strong ion gap, unmeasured anions, and the effects of sodium, chloride, phosphate, and albumin changes on ABE were calculated. Most parameters changed 20% in proportion to the magnitude of dehydration or hydration. Bicarbonate concentration, however, increased only 11% in the evaporation trial and decreased only -2% in the dehydration trial. The evaporation trial was associated with a mild, but significant, metabolic alkalotic effect (ABE increased 3.2 mM/L), whereas the hydration trial was associated with a slight, insignificant metabolic acidotic effect (ABE decreased only 0.6 mM/L). The calculated free water ABE effect (change in sodium concentration) was offset by opposite changes in calculated chloride, lactate, phosphate, and albumin ABE effects.

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Cobb male broiler chicks (1,000) on new litter were used to evaluate effects of dietary electrolyte balance [DEB; Na+K-Cl, milliequivalents (mEq) per kilogram] under tropical summer conditions. Corn-soybean meal-based mash diets had salt (NaCl) alone or in combination with one or more supplements: sodium bicarbonate (NaHCO3), ammonium chloride (NH4Cl), or potassium bicarbonate (KHCO3). A completely randomized design, with five starter and grower feed treatments (control: 145, then 130 mEq/kg; or 0, 120, 240, or 360 mEq/kg throughout) and four replicate pens (1.5 x 3.2 m) per treatment (50 chicks per pen), was used. Diets were analyzed for Na, K, and Cl for confirmation. There were no significant (P < 0.05) effects of treatments on mortality or processing parameters. Water intake increased linearly with increasing DEB, giving higher litter moistures and lower rectal temperatures. Blood HCO3 and pH increased with the highest DEB (360 mEq/kg) causing respiratory alkalosis. The DEB of 240 mEg/kg gave best weight gain and feed conversion ratio, and ideal DEB predicted by regression analyses were 186 and 197 mEq/kg from 0 to 21 d of age and 236 and 207 mEq/kg of feed from 0 to 42 d, respectively. These DEB corresponded to estimated (interpolated) values in predicted optimal 186 to 197 mEq/kg starter of Na 0.38 to 0.40% and Cl 0.405 to 0.39% (K = 0.52%), in 207 to 236 mEq/kg starter, Na 0.409 to 0.445% and Cl 0.326 to 0.372% Cl (K = 0.52%), and in grower Na 0.41 to 0.445%, Cl 0.315 to 0.267% (K = 0.47%).

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Individually caged male Cobb broilers (24), 44 d of age, were used to evaluate effects of heat stress (1 d of data collection) and dietary electrolyte balance (DEB; Na + K - Cl, mEq/kg from 1 d of age). During summer rearing, mortality was variable, but DEB 240 improved growth, feed conversion ratio, water intake, and waterrfeed ratio vs. DEB 0. The temperature sequence for heat stress was 24 to 32°C in 30 min, 32 to 36°C in 30 min, 36 to 37°C in 15 min, and 37 to 41°C in 45 min. Maximum temperature was held for 15, 60, 90, or 360 min for data collection (relative humidity averaged 42 ± 7%). Results from the same room before and after heat stress were analyzed by DEB (1-factor ANOVA) and before vs. after heat stress compared across DEB (2-sample t-test). Heat stress decreased blood Na, K, and pCO2, and lymphocytes but increased heterophils. Blood HCO3 rose, Cl declined, and hematocrit gave a concave pattern (lowest at DEB 120) as DEB increased. After heat stress, DEB O decreased blood Na and K, and DEB O and 120 levels decreased blood HCO3. After heat stress blood pCO2 and hemoglobin decreased with DEB 240, but it had highest pCO2, a key factor. The DEB 120 gave longest times to panting and prostration with DEB O and 240 results lower but similar statistically. In heat stress, DEB 360 was excessive, DEB 120 and 240 were favorable, and DEB 0 was intermediate based on hematology, panting, and prostration responses.

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This study correlated the solid preoperative fasting periods with plasma glycemia, serum cortisol, condition clinic and acid-base balance in dogs submitted to inhalation of general anaesthesia. Eight adults, animals were distributed into three groups in accordance with solid preoperative fasting: group 1 (12 hours), group 2 (18 hours) and group 3 (24 hours). Gastric emptying was observed and following this animals were submitted to the same anesthetic procedure. Heart and respiratory rate, rectal temperature, capillary refill time, percent hydration and noninvasive arterial pressure determined before and after Acepromazine and every 10 minutes during anaesthesia, included ETCO 2; values blood gas (pH, PaCO 2, PaO 2, HCO 3, TCO 2, SaO 2, BE), glycemic and serum cortisol were analyzed before MPA and each 30 minutes during anaesthesia. In recovery anaesthetic, glycemia and serum cortisol were repeated. During anaesthesia there were little cardiovascular and respiratory alteration not having interference of the preoperative fasting periods. Animals with 12 hours of the preoperative fasting showed a higher rise in glycemia levels than others groups in recovery anaesthetic. Serum cortisol wasn't influenced by fasting. Solid preoperative fasting independent of the duration describe a discreet respiratory alkalosis. All animals showed good clinical condition in all three groups. Solid preoperative fasting of the 18 hours is recommended to ensure a complete absence of the solid food contents in stomach.

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

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Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)

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Pós-graduação em Medicina Veterinária - FCAV