Both L- and D-Lactate Contribute to Metabolic Acidosis in Diarrheic Calves

Omole, Olutosin O; Nappert, Germain; Naylor, Jonathan M.; Zello, Gordon A.

doi:10.1093/jn/131.8.2128

Cited by 87 publications

(106 citation statements)

References 21 publications

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“…Elevated anion gap acidosis in calves with alimentary disorders generally was due to overproduction of organic acids. The most common anions found in such cases were lactate and keto acids (5,6,10). The results of our study indicate that AG correlated with lactate concentrations in serum only in the group of calves with diarrhea.…”

Section: Discussionmentioning

confidence: 48%

Analysis of acid–base disorders in calves with lactic acidosis using aclassic model and strong ion approach

Bednarski

Kupczyński²

2015

Turk J Vet Anim Sci

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IntroductionNeonatal calf diarrhea is a common disorder affecting calves and is an important cause of economic losses. The diarrhea of neonatal calves is usually associated with bacterial (enterotoxigenic strains of E. coli), rotaviral, and coronaviral infections and/or feeding factors (1,2). Clinical signs of diarrhea include loose watery stools, lack of appetite, and abdominal pain. This condition may result in dehydration, acid-base disorders, and electrolyte imbalances like metabolic acidosis, hyperkalemia, prolonged malnutrition, hypoglycemia, and hypothermia (3,4). The clinical status of an animal may further deteriorate due to lactic acidosis, which has been reported in diarrheic calves (5,6). Lactic acidosis is the result of elevated concentrations of L-lactate or/and D-lactate in the blood serum. L-lactate is produced by anaerobic metabolism due to tissue hypoperfusion or low oxygen supply to the tissue, while D-lactate is a byproduct of bacterial metabolism (5-7). Although levels of L-lactate or/and D-lactate can be elevated, only the nonstereospecific assay is routinely used in clinical practice.The interpretation of an acid-base balance is traditionally based on changes in pH, bicarbonate concentration (HCO 3 -), base excess (BE), and anion gap (AG) in plasma. This model characterizes four primary acid-base disturbances (i.e. respiratory acidosis and alkalosis, metabolic acidosis, and alkalosis) (8). The Stewart model (strong ion model) represents an alternative method of evaluation of acid-base status. This model is based on three independent variables to determine the acid-base balance: the strong ion difference (SID)-the difference between all completely dissociated cations and anions; the plasma partial pressure CO 2 (pCO 2 ), and the total nonvolatile weak acid concentration, mainly inorganic phosphate and albumin. The Stewart approach describes six primary acid-base disturbances (i.e. respiratory acidosis and alkalosis, strong ion acidosis and alkalosis, and nonvolatile buffer ion acidosis and alkalosis). Although the Stewart approach may give a better understanding of the mechanisms that underlie an acid-base disorder, the traditional methods are more convenient in daily practice (4,(8)(9)(10). Previous studies evaluated the use of two models for description of acid-base disturbances in cases of acute diarrhea, after intravenous fluid therapy or oral rehydration therapy (3,4,11,12).

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Section: Discussionmentioning

confidence: 48%

Analysis of acid–base disorders in calves with lactic acidosis using aclassic model and strong ion approach

Bednarski

Kupczyński²

2015

Turk J Vet Anim Sci

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“…The N group had higher blood HCO 3 -(33.0±4.33 mmol/L) than reported elsewhere (Oomole et al, 2001). However, the acidotic diets did not decrease HCO 3 -relative to the values measured in the N group.…”

Section: Advances In Animal and Veterinary Sciencescontrasting

confidence: 39%

Effect of Decreasing the Maize Content of Feed on Growth Performance, Rumen pH, and Blood Chemistry in Grain-Fed Holstein Bull Calves

Najid¹,

Couture²,

Chénier³

et al. 2017

Adv. Anim. Vet. Sci.

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“…9,[13][14][15][16] A decrease in plasma strong ion difference (SID; the difference in concentration between plasma strong cations and anions) directly causes a strong ion acidosis and acidemia. 17,18 Plasma SID is decreased by hyper-D-lactatemia, hyper-L-lactatemia, and hyponatremia accompanied by normochloremia or hyperchloremia; these changes are usually present in diarrheic calves.…”

mentioning

confidence: 99%

Use of a Quantitative Strong Ion Approach to Determine the Mechanism for Acid—Base Abnormalities in Sick Calves with or without Diarrhea

Constable

Stämpfli

Navetat³

et al. 2005

Veterinary Internal Medicne

112

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Acid-base abnormalities are frequently present in sick calves. The mechanism for an acid-base disturbance can be characterized using the strong ion approach, which requires accurate values for the total concentration of plasma nonvolatile buffers (A tot ) and the effective dissociation constant for plasma weak acids (K a ). The aims of this study were to experimentally determine A tot , K a , and net protein charge values for calf plasma and to apply these values quantitatively to data from sick calves to determine underlying mechanisms for the observed acid-base disturbance. Plasma was harvested from 9 healthy Holstein-Friesian calves and concentrations of quantitatively important strong ions (Na ϩ , K ϩ , Ca 2ϩ , Mg 2ϩ , Cl Ϫ , L-lactate) and nonvolatile buffer ions (total protein, albumin, phosphate) were determined. Plasma was tonometered with CO 2 at 37ЊC, and plasma PCO 2 and pH measured over a range of 15-159 mm Hg and 6.93-7.79, respectively. Strong ion difference (SID) was calculated from the measured strong ion concentrations, and nonlinear regression was used to estimate values for A tot and K a from the measured pH and PCO 2 and calculated SID. The estimated A tot and K a values were then validated using data from 2 in vivo studies. Mean (Ϯ SD) values for calf plasma were A tot ϭ 0.343 mmol/g of total protein or 0.622 mmol/g of albumin; K a ϭ (0.84 Ϯ 0.41) ϫ 10 Ϫ7 ; pK a ϭ 7.08. The net protein charge of calf plasma was 10.5 mEq/L, equivalent to 0.19 mEq/g of total protein or 0.34 mEq/g of albumin. Application of the strong ion approach to acid-base disturbances in 231 sick calves with or without diarrhea indicated that acidemia was due predominantly to a strong ion acidosis in response to hyponatremia accompanied by normochloremia or hyperchloremia and the presence of unidentified strong anions. These results confirm current recommendations that treatment of acidemia in sick calves with or without diarrhea should focus on intravenous or PO administration of a fluid containing sodium and a high effective SID.Key words: Calf diarrhea; D-lactic acidosis; Hyponatremia; Metabolic acidosis.A cidemia and metabolic acidosis occur commonly in sick calves with or without diarrhea. Metabolic acidosis in diarrheic calves was originally attributed to fecal bonate loss as well as the presence of unidentified organic acids in plasma and a decrease in glomerular filtration rate in response to severe dehydration.1-4 These proposed mechanisms for development of metabolic acidosis were based, in part, on the presence of hyper-L-lactatemia in diarrheic calves, 1,2,5,6 hyper-L-lactatemia and extensive loss of bicarbonate in the watery stool of humans with cholera, 7 and from (personal communication) of a high fecal bicarbonate concentration (40 mEq/L) in 4 calves with experimentally induced enterotoxigenic Escherichia coli diarrhea.c However, metabolic acidosis in diarrheic calves is probably predominantly due to causes other than fecal bicarbonate loss because diarrheic calves have measured mean daily fecal losses of s...

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Both L- and D-Lactate Contribute to Metabolic Acidosis in Diarrheic Calves

Cited by 87 publications

References 21 publications

Analysis of acid–base disorders in calves with lactic acidosis using aclassic model and strong ion approach

Analysis of acid–base disorders in calves with lactic acidosis using aclassic model and strong ion approach

Effect of Decreasing the Maize Content of Feed on Growth Performance, Rumen pH, and Blood Chemistry in Grain-Fed Holstein Bull Calves

Use of a Quantitative Strong Ion Approach to Determine the Mechanism for Acid—Base Abnormalities in Sick Calves with or without Diarrhea

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