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Forni, Lui G.; McKinnon, William; Hilton, P. J.

doi:10.1186/cc4954

Cited by 49 publications

(13 citation statements)

References 31 publications

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“…Evidence suggests that beside albumin, globulines and [P i ], also other weak and strong ions alter acid–base homeostasis during exercise (Forni et al 2006 ; McKinnon et al 2008 ). Particularly, amino acids, intermediates of the Krebs cycle, tricarboxylic acids and ammonia are released into the blood and may affect acid–base balance (Sewell et al 1994 ; Wagenmakers 1998 ; Casas et al 2001 ; Kato et al 2004 ).…”

Section: Discussionmentioning

confidence: 99%

“…The impact of this organic compound on acid–base homeostasis is not yet fully clarified. Several clinical and experimental studies suggest these organic compounds to be organic acids as well as ketone bodies and metabolic intermediates of the intracellular cycles of glucose and fatty acid metabolism (Forni et al 2006 ; Moviat et al 2008 ). McKinnon et al investigated this compound using liquid chromatography and enzyme assays (Forni et al 2006 ; McKinnon et al 2008 ).…”

Section: Discussionmentioning

confidence: 99%

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Changes in acid–base and ion balance during exercise in normoxia and normobaric hypoxia

et al. 2017

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PurposeBoth exercise and hypoxia cause complex changes in acid–base homeostasis. The aim of the present study was to investigate whether during intense physical exercise in normoxia and hypoxia, the modified physicochemical approach offers a better understanding of the changes in acid–base homeostasis than the traditional Henderson–Hasselbalch approach.MethodsIn this prospective, randomized, crossover trial, 19 healthy males completed an exercise test until voluntary fatigue on a bicycle ergometer on two different study days, once during normoxia and once during normobaric hypoxia (12% oxygen, equivalent to an altitude of 4500 m). Arterial blood gases were sampled during and after the exercise test and analysed according to the modified physicochemical and Henderson–Hasselbalch approach, respectively.ResultsPeak power output decreased from 287 ± 9 Watts in normoxia to 213 ± 6 Watts in hypoxia (−26%, P < 0.001). Exercise decreased arterial pH to 7.21 ± 0.01 and 7.27 ± 0.02 (P < 0.001) during normoxia and hypoxia, respectively, and increased plasma lactate to 16.8 ± 0.8 and 17.5 ± 0.9 mmol/l (P < 0.001). While the Henderson–Hasselbalch approach identified lactate as main factor responsible for the non-respiratory acidosis, the modified physicochemical approach additionally identified strong ions (i.e. plasma electrolytes, organic acid ions) and non-volatile weak acids (i.e. albumin, phosphate ion species) as important contributors.ConclusionsThe Henderson–Hasselbalch approach might serve as basis for screening acid–base disturbances, but the modified physicochemical approach offers more detailed insights into the complex changes in acid–base status during exercise in normoxia and hypoxia, respectively.Electronic supplementary materialThe online version of this article (doi:10.1007/s00421-017-3712-z) contains supplementary material, which is available to authorized users.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Changes in acid–base and ion balance during exercise in normoxia and normobaric hypoxia

et al. 2017

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“…Methanol, propylene glycol, ethylene glycol, salicylate, and some inborn error of metabolism are DOI: http://dx.doi.org/10.5772/intechopen.91760 other causes of unmeasured anions [33]. Both lactate and β-hydroxybutyrate are increased in both Gram-positive septiceamia [34] and starvation [35]. Krebs cycle intermediate citrate, isocitrate, malate, α-ketogluterate, succinate and D-lactate are increased in different types of acidosis.…”

Section: Unmeasured Anionmentioning

confidence: 99%

“…Krebs cycle intermediate citrate, isocitrate, malate, α-ketogluterate, succinate and D-lactate are increased in different types of acidosis. Intestinal ischemia and short bowel syndrome cause increase in D-lactate [35]. Plasma proteins are mostly anionic comprising 75% of the unmeasured anion [36][37][38].…”

Section: Unmeasured Anionmentioning

confidence: 99%

Acidosis and Anion Gap

Hassan¹

2021

New Insights Into Metabolic Syndrome

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The journey of exploring acid and base starts long before, but much advancement was seen in the last century. In 1890, Wilhelm Ostwald electronically measured hydrogen. Svante Arrhenius won the Noble prize in 1903 for the theory of ionization. In 1908, Henderson and Black showed that bicarbonate and phosphate equilibrate with CO 2 at normal body temperature. In 1923, Bronsted first put forward the idea of acid that ionizes in solution and donate hydrogen and the base accepts the hydrogen from the solution. Handerson invented the important bicarbonate buffer system and Hasselbalch First measured the actual blood pH. In 1909, S. P. S. Sorensen developed the pH scale. Later Hasselbalch-Henderson developed an equation that helped in relating pH to the blood bicarbonate and PCO 2. Acidosis has fatal consequences like CNS damage and death. Acidosis is rapidly stabilized by the body buffer systems. There are equal amounts of cations and anions in blood, but some of them are unmeasured. These unmeasured ions are mostly anions that produce an anion gap. Increased anion gap usually represents metabolic acidosis. Albumin and many other confounding factors influence the anion gap derangements. Accuracy in measuring anion gap is critically important for the evaluation of acidosis.

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“…High SAG is typical for the occurrence of unmeasured anions (for example ketones, lactate, metabolites of methanol and ethylene glycol, phosphate) where HCO 3− is consumed via its action as a buffer. High SAG metabolic acidosis is seen in ketoacidosis, lactic acidosis, intoxication and acute renal failure [ 2 ].…”

Section: Introductionmentioning

confidence: 99%

Renal tubular acidosis is highly prevalent in critically ill patients

et al. 2015

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IntroductionHyperchloremic acidosis is frequent in critically ill patients. Renal tubular acidosis (RTA) may contribute to acidemia in the state of hyperchloremic acidosis, but the prevalence of RTA has never been studied in critically ill patients. Therefore, we aimed to investigate the prevalence, type, and possible risk factors of RTA in critically ill patients using a physical-chemical approach.MethodsThis prospective, observational trial was conducted in a medical ICU of a university hospital. One hundred consecutive critically ill patients at the age ≥18, expected to stay in the ICU for ≥24 h, with the clinical necessity for a urinary catheter and the absence of anuria were included.Base excess (BE) subset calculation based on a physical-chemical approach on the first 7 days after ICU admission was used to compare the effects of free water, chloride, albumin, and unmeasured anions on the standard base excess. Calculation of the urine osmolal gap (UOG) - as an approximate measure of the unmeasured urine cation NH4+ - served as determinate between renal and extrarenal bicarbonate loss in the state of hyperchloremic acidosis.ResultsDuring the first week of ICU stay 43 of the patients presented with hyperchloremic acidosis on one or more days represented as pronounced negative BEChloride. In 31 patients hyperchloremic acidosis was associated with RTA characterized by a UOG ≤150 mosmol/kg in combination with preserved renal function. However, in 26 of the 31 patients with RTA metabolic acidosis was neutralized by other acid-base disturbances leading to a normal arterial pH.ConclusionsRTA is highly prevalent in critically ill patients with hyperchloremic acidosis, whereas it is often neutralized by the simultaneous occurrence of other acid-base disturbances.Trial registrationClinicaltrials.gov NCT02392091. Registered 17 March 2015

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Untitled

Cited by 49 publications

References 31 publications

Changes in acid–base and ion balance during exercise in normoxia and normobaric hypoxia

Changes in acid–base and ion balance during exercise in normoxia and normobaric hypoxia

Acidosis and Anion Gap

Renal tubular acidosis is highly prevalent in critically ill patients

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