921 resultados para acid base balance
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Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)
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Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)
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Pós-graduação em Medicina Veterinária - FCAV
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Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)
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Zagatto, AM, Padulo, J, Muller, PTG, Miyagi, WE, Malta, ES, and Papoti, M. Hyperlactemia induction modes affect the lactate minimum power and physiological responses in cycling. J Strength Cond Res 28(10): 2927-2934, 2014The aim of this study was to verify the influence of hyperlactemia and blood acidosis induction on lactate minimum intensity (LMI). Twenty recreationally trained males who were experienced in cycling (15 cyclists and 5 triathletes) participated in this study. The athletes underwent 3 lactate minimum tests on an electromagnetic cycle ergometer. The hyperlactemia induction methods used were graded exercise test (GXT), Wingate test (WAnT), and 2 consecutive Wingate tests (2 x WAnTs). The LMI at 2 x WAnTs (200.3 +/- 25.8 W) was statistically higher than the LMI at GXT (187.3 +/- 31.9 W) and WAnT (189.8 +/- 26.0 W), with similar findings for blood lactate, oxygen uptake, and pulmonary ventilation at LMI. The venous pH after 2 x WAnTs was lower (7.04 +/- 0.24) than in (p <= 0.05) the GXT (7.19 +/- 0.05) and WAnT (7.19 +/- 0.05), whereas the blood lactate response was higher. In addition, similar findings were observed for bicarbonate concentration [HCO3] (2 x WAnTs lower than WAnT; 15.3 +/- 2.6 mmol center dot L-1 and 18.2 +/- 2.7 mmol center dot L(-)1, respectively) (p <= 0.05). However, the maximal aerobic power and total time measured during the incremental phase also did not differ. Therefore, we can conclude that the induction mode significantly affects pH, blood lactate, and [HCO3] and consequently they alter the LMI and physiological parameters at LMI.
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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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The aim of this study was to evaluate the blood gas profile of experimentally copper-poisoned sheep (in the pre-hemolytic, hemolytic and post-hemolytic phases) that have been treated or not treated with ammonium tetrathiomolybdate. Ten lambs of the Santa Ines breed were divided into two groups: control and ATTM (treated (ammonium tetrathiomolibydate). The animals were submitted to increasing doses of copper sulfate until macroscopic hemoglobinuria was detected. All of the control animals from died within four days of hemolytic crisis, and one sheep from ATTM died during the treatment. There was no difference in blood gas parameters between experimental groups. Higher values of pCO(2) were observed during the hemolytic crisis (HC) in both groups. The control group had higher mean values of hCO(3) in the times HC and 2 days after hemolytic crisis (dA) when compared with the time 15 before hemolytic crises (dB). The sheep that were treated with ATTM presented lower values of hCO(3) at 7dB and higher levels at the HC. The control and ATTM groups exhibited higher values of BE during the HC. Poisoning resulted in disorder in the acid-base equilibrium, characterized by metabolic alkalosis and respiratory acidosis. Treatment with ATTM was able to reverse the changes in acid-base balance in copper poisoning sheep.
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[EN] With altitude acclimatization, blood hemoglobin concentration increases while plasma volume (PV) and maximal cardiac output (Qmax) decrease. This investigation aimed to determine whether reduction of Qmax at altitude is due to low circulating blood volume (BV). Eight Danish lowlanders (3 females, 5 males: age 24.0 +/- 0.6 yr; mean +/- SE) performed submaximal and maximal exercise on a cycle ergometer after 9 wk at 5,260 m altitude (Mt. Chacaltaya, Bolivia). This was done first with BV resulting from acclimatization (BV = 5.40 +/- 0.39 liters) and again 2-4 days later, 1 h after PV expansion with 1 liter of 6% dextran 70 (BV = 6.32 +/- 0.34 liters). PV expansion had no effect on Qmax, maximal O2 consumption (VO2), and exercise capacity. Despite maximal systemic O2 transport being reduced 19% due to hemodilution after PV expansion, whole body VO2 was maintained by greater systemic O2 extraction (P < 0.05). Leg blood flow was elevated (P < 0.05) in hypervolemic conditions, which compensated for hemodilution resulting in similar leg O2 delivery and leg VO2 during exercise regardless of PV. Pulmonary ventilation, gas exchange, and acid-base balance were essentially unaffected by PV expansion. Sea level Qmax and exercise capacity were restored with hyperoxia at altitude independently of BV. Low BV is not a primary cause for reduction of Qmax at altitude when acclimatized. Furthermore, hemodilution caused by PV expansion at altitude is compensated for by increased systemic O2 extraction with similar peak muscular O2 delivery, such that maximal exercise capacity is unaffected.
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Clinical studies evaluating the use of phenylephrine in septic shock are lacking. The present study was designed as a prospective, crossover pilot study to compare the effects of norepinephrine (NE) and phenylephrine on systemic and regional hemodynamics in patients with catecholamine-dependent septic shock. In 15 septic shock patients, NE (0.82 +/- 0.69 mug.kg.min) was replaced with phenylephrine (4.39 +/- 5.23 mug.kg.min) titrated to maintain MAP between 65 and 75 mmHg. After 8 h of phenylephrine infusion treatment was switched back to NE. Data from right heart catheterization, acid-base balance, thermo-dye dilution catheter, gastric tonometry, and renal function were obtained before, during, and after replacing NE with phenylephrine. Variables of systemic hemodynamics, global oxygen transport, and acid-base balance remained unchanged after replacing NE with phenylephrine except for a significant decrease in heart rate (phenylephrine, 89 +/- 18 vs. NE, 93 +/- 18 bpm; P < 0.05). However, plasma disappearance rate (phenylephrine, 13.5 +/- 7.1 vs. NE, 16.4 +/- 8.7%.min) and clearance of indocyanine green (phenylephrine, 330 +/- 197 vs. NE, 380 +/- 227mL.min.m), as well as creatinine clearance (phenylephrine, 81.3 +/- 78.4 vs. NE, 94.3 +/- 93.5 mL.min) were significantly decreased by phenylephrine infusion (each P < 0.05). In addition, phenylephrine increased arterial lactate concentrations as compared with NE infusion (1.7 +/- 1.0 vs. 1.4 +/- 1.1 mM; P < 0.05). After switching back to NE, all variables returned to values obtained before phenylephrine infusion except creatinine clearance and gastric tonometry values. Our results suggest that for the same MAP, phenylephrine causes a more pronounced hepatosplanchnic vasoconstriction as compared with NE.
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BACKGROUND The metabolism of sodium, potassium, and chloride and the acid-base balance are sometimes altered in cystic fibrosis. Textbooks and reviews only marginally address the homeostasis of magnesium in cystic fibrosis. METHODS We performed a search of the Medical Subject Headings terms (cystic fibrosis OR mucoviscidosis) AND (magnesium OR hypomagnes[a]emia) in the US National Library of Medicine and Excerpta Medica databases. RESULTS We identified 25 reports dealing with magnesium and cystic fibrosis. The results of the review may be summarized as follows. First, hypomagnesemia affects more than half of the cystic fibrosis patients with advanced disease; second, magnesemia, which is normally age-independent, relevantly decreases with age in cystic fibrosis; third, aminoglycoside antimicrobials frequently induce both acute and chronic renal magnesium-wasting; fourth, sweat magnesium concentration was normal in cystic fibrosis patients; fifth, limited data suggest the existence of an impaired intestinal magnesium balance. Finally, stimulating observations suggest that magnesium supplements might achieve an improvement in respiratory muscle strength and mucolytic activity of both recombinant and endogenous deoxyribonuclease. CONCLUSIONS The first comprehensive review of the literature confirms that, despite being one of the most prevalent minerals in the body, the importance of magnesium in cystic fibrosis is largely overlooked. In these patients, hypomagnesemia should be sought once a year. Furthermore, the potential of supplementation with this cation deserves more attention.
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The impact of the chemical changes in the ocean waters due to the increasing atmospheric CO2 depends on the ability of an organism to control extracellular pH. Among sea urchins, this seems specific to the Euechinoidea, sea urchins except Cidaroidea. However, Cidaroidea survived two ocean acidification periods: the Permian-Trias and the Cretaceous-Tertiary crises. We investigated the response of these two sea urchin groups to reduced seawater pH with the tropical cidaroid Eucidaris tribuloides, the sympatric euechinoid Tripneustes ventricosus and the temperate euechinoid Paracentrotus lividus. Both euechinoid showed a compensation of the coelomic fluid pH due to increased buffer capacity. This was linked to an increased concentration of DIC in the coelomic fluid and thus of bicarbonate ions (most probably originating from the surrounding seawater as isotopic signature of the carbon -delta 13C- was similar). On the other hand, the cidaroid showed no changes within the coelomic fluid. Moreover, the delta 13C of the coelomic fluid did not match that of the seawater and was not significantly different between the urchins from the different treatments. Feeding rate was not affected in any species. While euechinoids are able to regulate their extracellular acid-base balance, many questions are still unanswered on the costs of this capacity. On the contrary, cidaroids do not seem affected by a reduced seawater pH. Further investigations need to be undertaken to cover more species and physiological and metabolic parameters in order to determine if energy trade-offs occur and how this mechanism of compensation is distributed among sea urchins.
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The effect of short-term (5 days) exposure to CO2-acidified seawater (year 2100 predicted values, ocean pH = 7.6) on key aspects of the function of the intertidal common limpet Patella vulgata (Gastropoda: Patellidae) was investigated. Changes in extracellular acid-base balance were almost completely compensated by an increase in bicarbonate ions. A concomitant increase in haemolymph Ca2+ and visible shell dissolution implicated passive shell dissolution as the bicarbonate source. Analysis of the radula using SEM revealed that individuals from the hypercapnic treatment showed an increase in the number of damaged teeth and the extent to which such teeth were damaged compared with controls. As radula teeth are composed mainly of chitin, acid dissolution seems unlikely, and so the proximate cause of damage is unknown. There was no hypercapnia-related change in metabolism (O2 uptake) or feeding rate, also discounting the possibility that teeth damage was a result of a CO2-related increase in grazing. We conclude that although the limpet appears to have the physiological capacity to maintain its extracellular acid-base balance, metabolism and feeding rate over a 5 days exposure to acidified seawater, radular damage somehow incurred during this time could still compromise feeding in the longer term, in turn decreasing the top-down ecosystem control that P. vulgata exerts over rocky shore environments.
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Ocean acidification has a wide-ranging potential for impacting the physiology and metabolism of zooplankton. Sufficiently elevated CO2 concentrations can alter internal acid-base balance, compromising homeostatic regulation and disrupting internal systems ranging from oxygen transport to ion balance. We assessed feeding and nutrient excretion rates in natural populations of the keystone species Euphausia superba (Antarctic krill) by conducting a CO2 perturbation experiment at ambient and elevated atmospheric CO2 levels in January 2011 along the West Antarctic Peninsula (WAP). Under elevated CO2 conditions (~672 ppm), ingestion rates of krill averaged 78 µg C/individual/d and were 3.5 times higher than krill ingestion rates at ambient, present day CO2 concentrations. Additionally, rates of ammonium, phosphate, and dissolved organic carbon (DOC) excretion by krill were 1.5, 1.5, and 3.0 times higher, respectively, in the high CO2 treatment than at ambient CO2 concentrations. Excretion of urea, however, was ~17% lower in the high CO2 treatment, suggesting differences in catabolic processes of krill between treatments. Activities of key metabolic enzymes, malate dehydrogenase (MDH) and lactate dehydrogenase (LDH), were consistently higher in the high CO2 treatment. The observed shifts in metabolism are consistent with increased physiological costs associated with regulating internal acid-base equilibria. This represents an additional stress that may hamper growth and reproduction, which would negatively impact an already declining krill population along the WAP.
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With global climate change, ocean warming and acidification occur concomitantly. In this study, we tested the hypothesis that increasing CO2 levels affect the acid-base balance and reduce the activity capacity of the Arctic spider crab Hyas araneus, especially at the limits of thermal tolerance. Crabs were acclimated to projected oceanic CO2 levels for 12 days (today: 380, towards the year 2100: 750 and 1,120 and beyond: 3,000 ?atm) and at two temperatures (1 and 4 °C). Effects of these treatments on the righting response (RR) were determined (1) at acclimation temperatures followed by (2) righting when exposed to an additional acute (15 min) heat stress at 12 °C. Prior to (resting) and after the consecutive stresses of combined righting activity and heat exposure, acid-base status and lactate contents were measured in the haemolymph. Under resting conditions, CO2 caused a decrease in haemolymph pH and an increase in oxygen partial pressure. Despite some buffering via an accumulation of bicarbonate, the extracellular acidosis remained uncompensated at 1 °C, a trend exacerbated when animals were acclimated to 4 °C. The additional combined exposure to activity and heat had only a slight effect on blood gas and acid-base status. Righting activity in all crabs incubated at 1 and 4 °C was unaffected by elevated CO2 levels or acute heat stress but was significantly reduced when both stressors acted synergistically. This impact was much stronger in the group acclimated at 1 °C where some individuals acclimated to high CO2 levels stopped responding. Lactate only accumulated in the haemolymph after combined righting and heat stress. In the group acclimated to 1 °C, lactate content was highest under normocapnia and lowest at the highest CO2 level in line with the finding that RR was largely reduced. In crabs acclimated to 4 °C, the RR was less affected by CO2 such that activity caused lactate to increase with rising CO2 levels. In line with the concept of oxygen and capacity limited thermal tolerance, all animals exposed to temperature extremes displayed a reduction in scope for performance, a trend exacerbated by increasing CO2 levels. Additionally, the differences seen between cold- and warm-acclimated H. araneus after heat stress indicate that a small shift to higher acclimation temperatures also alleviates the response to temperature extremes, indicating a shift in the thermal tolerance window which reduces susceptibility to additional CO2 exposure.