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At least 19 recordsLinked to original sources
PubMed1979

Lactate-to-pyruvate or pyruvate-to-lactate assay for lactate dehydrogenase: a re-examination.

The pyruvate-to-lactate assay for determining lactate dehydrogenase (EC 1.1.1.27) can now yield linearity equal to or better than that obtained by the lactate-to-pyruvate assay. In addition, there are significant advantages to the pyruvate-to-lactate reaction: (a) a greater change in absorbance per unit time, which allows more accurate spectrophotometric readout; (b) lower reactant concentrations are required, which substantially reduces the cost per assay; (c) solid reagents are used to prepare the assay solution; and (d) reagent solutions are more stable. However, impurities present in commercial NADH preparations may substantially affect measured lactated dehydrogenase activities; therefore, a Standard Reference Material for NADH is being developed for issuance by the National Bureau of Standards.

L-Lactate Dehydrogenase↗
PubMed1978

Optimal conditions and comparison of lactate dehydrogenase catalysis of the lactate-to-pyruvate and pyruvate-to-lactate reactions in human serum at 25, 30, and 37 degrees C.

We report optimal conditions for assaying highly purified human lactate dehydrogenase isoenzymes with the lactate-to-pyruvate and pyruvate-to-lactate reactions, as they apply to human serum. Interconversion of results between reactions is not practicable. Measurements of lactate dehydrogenase in either reaction direction at 25, 30, or 37 degrees C can be equally reliable if the volume fraction and the resulting deltaA/min is small. However, for interinstrument and interlaboratory comparisons, results from the lactate-to-pyruvate reaction are more reliable.

Buffers↗
PubMed1977

Optimal conditions for assaying human lactate dehydrogenase by the lactate-to-pyruvate reaction: Arrhenium relationships for lactate dehydrogenase isoenzymes 1 and 5.

Optimal reaction conditions to sassay human lactate dehydrogenase (lactate-to-pyruvate) were established for isoenzymes 1 and 5 at 25, 30, and 37 degrees C in diethanolamine and 2-amino-2-methyl-1,3-propanediol. Different substrate concentrations are required at each temperature. The conditions permit measurement of lactate dehydrogenase 1 and 5 with the lowest substrate concentrations that allow for the highest equal sustainable efficiency in measuring both isoenzymes. About 95% of each isoenzyme activity is measured if the assay is performed within the first minute after the reaction is initiated even for activities as high as triple the upper limit of normal. The Arrhenius relationship is different for each isoenzyme, but results obtained for each at one temperature can be compared with results at another temperature by use of simple conversion equations. Assays at 25 and 30 degrees C are more economical and less variable than assays at 37 degrees C.

Buffers↗
PubMed1992

Effects of sodium L-lactate and sodium racemic lactate on intraoperative acid-base status.

Lactated Ringer's solution is frequently used to avoid metabolic acidosis during fluid resuscitation. The standard lactated Ringer's solution contains racemic lactate, an equal mixture of the D- and L-stereoisomers. We investigated whether sodium L-lactate or sodium racemic lactate (DL-lactate) is more effective for increasing buffering capacity in body fluids. For the purpose of this comparison, Ringer's solutions containing no lactate, sodium L-lactate, or racemic lactate at a concentration of 84 mEq/L (three times more than the ordinary level) were infused in patients under general anesthesia during tympanoplasty. Although differences occurred among the three groups in blood concentrations of L-lactate, D-lactate, and the L-lactate/pyruvate ratio, no differences occurred between the two lactate groups in either bicarbonate ion concentration or base excess. The amount of buffering capacity increased significantly in both lactate groups, compared with preinfusion levels, and was more than the values in the nonlactated Ringer's solution group. We conclude that sodium racemic lactate is metabolized at nearly the same rate as that of sodium L-lactate.

Acid-Base Equilibrium↗
PubMed1979

Lactate elimination in man: effects of lactate concentration and hepatic dysfunction.

Lactate elimination was studied in twenty-six healthy volunteers during primed constant lactate infusion or multiple lactate injection tests, at blood lactate concentrations of 1-8 mmol-1. Although lactate elimination fitted a single exponential curve over a 30 min period, a significant correlation between the rate removal constant (KL) and the peak blood lactate concentration (Lphi) was demonstrated: loge KL = -2.43-0.132 Lphi (P = 0.003, r = 0.63, n = 20) This suggests that lactate removal does not follow first order kinetics over a wide concentration range but becomes saturated at relatively low blood lactate concentrations. Estimates of the lactate distribution volume did not differ significantly at different dosage levels, but remained in the range 270-300 ml kg-1. Skeletal muscle uptake accounted for about 26% of the infused lactate load. Seven patients with well-compensated hepatic cirrhosis were compared with a group of six control subjects during primed constant infusion tests. Fasting and steady state blood lactate concentrations achieved were similar in both groups. A significant prolongation in lactate half-life was demonstrated in the cirrhotics (18.8 +/- 1.4 min (mean +/- SEM) compared to 14.7 +/- 2.2 min; P less than 0.02). Since peripheral uptake of lactate in the forearm was similar in the two groups, this suggests that hepatic lactate uptake was impaired, due either to hepatocyte dysfunction or portal diversion.

Adult↗
PubMed1992

Insulin resistance in obesity is associated with elevated basal lactate levels and diminished lactate appearance following intravenous glucose and insulin.

Lactate metabolism is altered in obesity. Increasing obesity is associated with increased blood lactate levels after an overnight fast. In contrast, we have recently shown a marked decrease in the capacity for acute lactate generation in obese subjects following an oral glucose load, which we postulated might be linked to altered insulin sensitivity. In the present study, we systematically analyzed the relationship between insulin sensitivity (the Sensitivity Index [SI] derived using the minimal model), body mass index (BMI), and glucose, insulin, and lactate levels in the basal state and following intravenous (IV) glucose and insulin administration in lean and obese subjects. The results showed that SI and BMI were inversely related, as expected. Insulin sensitivity was more tightly associated with glucose, insulin, and lactate levels (both basal and integrated) than obesity per se. A significant inverse relationship was found between SI and basal lactate levels (r = -.56). Moreover, a significant and positive relationship was found between SI and incremental lactate area under the curve (reflecting acute lactate production) (r = .41). In a multiple regression analysis to separate the independent effects of obesity (BMI) and insulin sensitivity, after adjusting for age, sex, and race, SI accounted for 34% of the variance in basal lactate and 24% of the variance in incremental lactate area. Obesity independently accounted for 10% of the variance in basal lactate and 11% of the variance in incremental lactate area, neither of which were statistically significant. We conclude that elevations in basal lactate are associated with the development of insulin resistance.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1975

Relationship of lactate dehydrogenase specificity and growth rate to lactate metabolism by Selenomonas ruminantium.

A lactate-fermenting strain of Selenomonas ruminantium (HD4) and a lactatenonfermenting strain (GA192) were examined with respect to the stereoisomers of lactate formed during glucose fermentation, the stereoisomers of lactate fermented by HD4, and the characteristics of the lactate dehydrogenases of the strains. GA192 formed L-lactate and HD4 formed L-lactate and small amounts of D-lactate from glucose. HD4 fermended L- but not D-lactate. Both strains contain nicotinamide adenine dinucleotide (NAD)-specific lactate dehydrogenases, and no NAD-independent lactate oxidation was detected. Continuous cultures of both strains grown with limiting glucose produced mainly propionate and acetate and little lactate at dilution rates less than 0.4/h, with shifts to increasing amounts of lactate and less acetate and propionate as the dilution rate was increased from 0.4/h to approximately 1/h.

Acetates↗
PubMed1979

Differences between lactating and non-lactating dairy cows in concentration and secretion rate of insulin.

1. Four parameters of insulin metabolism were compared in catheterized lactating and non-lactating Friesian x Ayrshire dairy cows. 2. The four parameters, i.e. arterial and portal-venous concentrations of insulin, and pancreatic output and hepatic uptake of insulin, were approx. 2-, 3-, 3- and 5-fold higher respectively in the non-lactating cows than in the lactating cows in the normal fed state. Statistical significance was not achieved for the differences in magnitude in the case of the latter two parameters, however. 3. All four parameters increased significantly about 4-fold when non-lactating cows were infused intravenously with glucose for 48 h at a rate of 4.2 mmol/min. The parameters also increased in the lactating cows during glucose infusion, but the values reached were substantially lower than in the non-lactating cows and the increases were not statistically significant. 4. Arterial insulin concentrations doubled in the non-lactating cows during a 3 h infusion of propionate into a mesenteric vein, but remained unaltered in the lactating cows. 5. Differences in insulin concentration and output between the lactating and non-lactating cows were not consistently related to differences in either glucose concentration or glucose-entry rate. Arterial propionate concentrations were similar in both groups of cows at all times. 6. It is concluded that in the dairy cow, insulin secretion in response to an insulinotropic agent is diminished during lactation.

Animals↗
PubMed1992

Metabolism of pregnant-lactating rats is adapted to pregnancy rather than to lactation.

In pregnant-lactating rats implantation was induced on day 4 of lactation so that, as an exception, lactation coincided with the period of high fetal growth. The already present suckling litters of these animals lagged behind in growth, but the "second" litters were at birth normal in size and weight. Such pregnant-lactating rats were tested in vivo with intravenous glucose loads and compared with cyclic and lactating rats. Glucose tolerance was unaffected by the reproductive state. Pregnant-lactating rats showed, just as during their first pregnancy, low basal glucose levels. Their basal insulin levels and insulin responses, however, were decreased in comparison with the first pregnancy and resembled those of lactating rats. This may be due to an increased insulin turnover, because in vitro insulin responsiveness and insulin content of both "pregnant-lactating" and "pregnant" islets were increased in comparison with "cyclic" and "lactating" islets. It was concluded that the metabolism of pregnant-lactating rats is adapted to the pregnant rather than to the lactational state.

Adaptation, Physiological↗
PubMed1992

Effects of sodium lactate infusion on cisternal lactate and carbon dioxide levels in nonhuman primates.

OBJECTIVE: To further the understanding of lactate-induced panic in patients with panic disorder, the authors examined cisternal lactate and carbon dioxide levels in nonhuman primates after infusions of sodium lactate comparable to those used in studies of human beings. METHOD: CSF and venous blood lactate, pH, PCO2, PO2, and bicarbonate were measured in five ketamine-anesthetized nonhuman primates, without mechanical ventilation, before and after they underwent infusions of sodium lactate. In addition, the same measurements were made for three of the five subjects who were given saline infusions. RESULTS: Despite the development of the characteristic peripheral biochemical effects of infused sodium lactate--increased lactate and bicarbonate levels and metabolic alkalosis--no increases in central lactate or carbon dioxide levels were observed. Saline infusions produced no biochemical effects on venous and cisternal measures. CONCLUSIONS: The results of this study are in keeping with previous findings of nonpermeability of the blood-brain barrier to anionic compounds such as lactate. They therefore support theories of lactate panic based on cognitive and/or brainstem misevaluation of peripheral somatic sensations.

Animals↗
PubMed1992

Is accelerated oxidation of lactate required for dichloroacetate to lower the level of lactate in blood?

We examined mechanisms by which dichloroacetate (DCA), an activator of pyruvate dehydrogenase (PDH), led to a decrease in the concentration of lactate in blood in a unique "metabolic setting," where the concentration of lactate in blood was 5.4 +/- 0.5 mmol/L. Elevated levels of lactate were induced in anaesthetized rabbits by the administration of a large dose of insulin. The rate of consumption of oxygen was 1.2 +/- 0.1 mmol/min, the respiratory quotient was close to unity, and close to half of the PDH was in its active form; therefore, virtually all ATP synthesis should require flux through PDH. Hence, we predicted that DCA should not cause a significant decrease in the concentration of lactate in blood in this model. In contrast, if DCA was effective, new insights could be obtained into its mechanisms of action, at least in this setting. During steady-state hyperlactatemia, DCA was given as its sodium salt, 2 mmol/kg (n = 10); a control group (n = 5) received equimolar NaCl. Forty minutes later, the level of lactate in blood in the DCA group was 1.3 +/- 0.2 mmol/L, significantly lower than in the NaCl group (4.2 +/- 0.6 mmol/L). To determine the organ(s) responsible for removing lactate, arteriovenous differences were measured in organs drained by the jugular, femoral, and hepatic veins. There was no net uptake of lactate in these drainage beds after DCA was administered. From a quantitative analysis of the rate of removal of lactate and the rate of consumption of oxygen, it seems unlikely that the majority of the decrease in lactate could be directly attributed to an increase in its oxidation.

Animals↗
PubMed1977

[Blood picture in lactate acidosis. Part 2: acid-base equilibrium and lactate].

A differentiation between lactate emia (lactic acid emia) and lactate acidosis (lactic acidosis) is made. The normal value for blood lactate concentration is 1-2 mmol/1. The term lactate emia is used for lactate values between 2-6 mmol/1. The limiting value for the diagnosis of lactate acidosis should be more than 7-8 mmol/1 for the blood lactate concentration. Furthermore the different buffer mechanisms are evaluated in respect to their influence on the pH of the blood and to lactate metabolism. Especially the mechanism of respiratory compensation for metabolic acidosis is discussed. It is stated that for the diagnosis of lactate acidosis the blood-pH and the bicarbonate concentration should be measured.

Acid-Base Equilibrium↗
PubMed1992

MRS detection of whole brain lactate rise during 1 M sodium lactate infusion in rats.

Proton magnetic resonance spectroscopy (1H MRS) performed in vivo on nine Sprague Dawley rats detected a threefold increase in whole brain lactate during intravenous 1 mol/L sodium lactate infusion. Significant increases in whole brain lactate were detected within 5 min after starting lactate infusion, progressively rose to a maximum level estimated at 3.2 +/- 1.5 mmol/L (all values +/- SD) immediately postinfusion, then decreased towards baseline levels during the next hr. Venous lactate concentration, increasing from 2.3 +/- 2.4 mmol/L to 43.0 +/- 8.0 mmol/L during the infusion, exhibited a steeper rise and then decreased more rapidly in comparison to changes in whole brain lactate. These data suggest MRS can be used in vivo to study acute changes in brain lactate associated with increasing blood lactate concentrations.

Animals↗
PubMed1992

Localized magnetic resonance spectroscopy measurement of brain lactate during intravenous lactate infusion in healthy volunteers.

Proton magnetic resonance spectroscopy (1H MRS) localized to the left temporal-parietal region in 8 healthy volunteers detected a 2.1-fold +/- 0.7-fold increase (all values +/-SD) in brain lactate during intravenous infusion of 0.5 molar (M) sodium lactate (5 meq/kg over 20 minutes). Significant increases in brain lactate occurred within 5-10 minutes after starting lactate infusion, progressively rose during the infusion, then decreased towards baseline levels during 30 minutes post-infusion. Venous lactate concentration increased from 0.8 +/- 0.2 mM to 10.9 +/- 4.1 mM or 13.6-fold during the infusion. Flow phantom findings in vitro suggest attenuation of 1H MRS blood lactate signal from arteries and veins as a result of flow velocity effects. Correlations between paired blood and brain lactate measurements at each sampling time indicate a non-linear relationship between compartments during lactate infusion.

Adult↗
PubMed1978

Lactate release in relation to tissue lactate in human skeletal muscle during exercise.

In four healthy volunteers, muscle lactate concentration and the release of lactate from the leg were determined at rest and at 4 and 12 min of sitting bicycle exercise at four intensities (30, 50, 70, and 90% of maximal oxygen uptake). The muscle biopsies were obtained by needle biopsy technique from m. vastus lateralis. The rate of lactate release was calculated from the femoral venous-arterial differences of lactate and the leg blood flow was determined by constant rate dye infusion. Both leg blood flow and leg oxygen consumption increased linearly with work intensity. The release of lactate rose approximately linearly with the muscle lactate concentration up to about 4-5 mmol/min but then the relationship revealed a clear leveling off. These results indicate a maximal level for the lactate release from the exercising muscles with a translocation hindrance for lactate within the muscles.

Adult↗
PubMed1992

[Development of automated lactate analyzer with continuous blood sampling for monitoring blood lactate and its application for the testing of physical exercise].

The anaerobic threshold is useful for estimating the intensity of physical exercise. It is shown as either an increase in blood concentrations of lactate or a disproportionate increase in ventilation. We developed a lactate analyzer based on an electroenzymatic method with a continuous blood sampling system through a double-lumen catheter. Ascorbic acid, bilirubin, hemoglobin, creatinine, uric acid, and glucose did not interfere the results. The lactate concentrations in blood samples from healthy subjects during physical exercise correlated well (r = 0.993) with results measured by the conventional enzymatic method. We measured the concentrations of blood lactate with a use of this lactate analyzer to see the anaerobic threshold in nine healthy volunteers during exercise on a treadmill with an increasing workload. The point at which lactate concentrations started to increase was detected easily. The anaerobic threshold identified as a disproportionate increase in ventilation was seen at almost the same time. We conclude that the lactate analyzer, with a continuous blood sampling system, can measure precisely concentrations of lactate in blood and can detect the anaerobic threshold during physical exercise.

Adult↗