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PubMed2005

L-lactate measures in brain tissue with ceramic-based multisite microelectrodes.

A newly developed multisite array microelectrode for in vivo measurements of L-lactate is presented. The resulting microelectrode is composed of three functional layers. First, Nafion is used to repel interfering electroactive anions, such as ascorbate. Second, L-lactate oxidase immobilized onto the recording sites is used to convert L-lactate to hydrogen peroxide. The H2O2 produced is proportional to L-lactate concentrations and is quantified at the platinum recording sites. Third, a layer of polyurethane is coated over the L-lactate oxidase to adjust the linear range of the microelectrode to one that is compatible with in vivo measurements. This layer reduces the amount of L-lactate that diffuses to the enzyme while not significantly limiting oxygen diffusion. The resulting L-lactate microelectrodes were linear to 20 mM (R2 = 0.997 +/- 0.001) and beyond in some cases with detection limits of 0.078 +/- 0.013 mM (n = 12). The selectivity and response time of these electrodes make them suitable for in vivo measurements in brain tissue. Self-referencing recordings may be utilized to further improve the selectivity of the recordings. However this is not necessary for most applications in the brain, because the resting and stimulated levels of dopamine (DA), norepinephrine (NE), and other potentially interfering cations are two to three orders of magnitude lower than that of in vivo L-lactate, which is in the millimolar range. Preliminary in vivo measures of L-lactate in the brain of anesthetized rats support that the microelectrodes are capable of measuring rapid endogenous changes in vivo.

Animals↗
PubMed2005

Lactate: early predictor of morbidity and mortality in patients with severe burns.

A severe burn results in a devastating and unique derangement called burn shock. Historically, resuscitation has been guided by a combination of basic laboratory values, invasive monitoring and clinical findings, but the optimal guide to the endpoint of resuscitation remains controversial. One-hundred sixty-six patients, who were admitted to our Burn Unit, were enrolled in this prospective study. Resuscitation of these patients was undertaken according to the current standard of care. Parkland formula was used as a first approximation of acquired fluid administration rates and fluid administration was adapted in order to meet clinical needs. The aim of this study was to evaluate if plasma lactate is a useful parameter to estimate the severity of a burn shock. One of the main objectives was to evaluate, if the lactate clearance adds additional information. The results of this study indicate that the initial lactate level (Day 0) is a useful parameter to separate survivors from non-survivors. Moreover, a significant marker of shock and resuscitation was observed in evaluating the lactate clearance on Day 1. A better chance of survival occurs when resuscitation results in a lactate clearance to normal values within 24h (survival was 68% if the lactate reached normal values, compared to 32% if the lactate level remained supra-normal). In summary, we believe that measuring lactate and lactate clearance may help to detect critically injured patients either for adequacy of treatment, or selection of other therapeutic options.

Biomarkers↗
PubMed2005

Postoperative lactate concentrations predict the outcome of infants aged 6 weeks or less after intracardiac surgery: a cohort follow-up to 18 months.

OBJECTIVES: An observational cohort study was conducted in infants less than 6 weeks of age undergoing intracardiac surgery to examine the predictive value of serial postoperative lactate determination on survival and early childhood neurodevelopment. METHODS: A total of 85 infants with congenital heart disease underwent intracardiac surgery between 1996 and 1999. Differences in serial lactate concentrations after surgery among 3 outcome groups were compared. The predictive value of plasma lactate concentration on outcome (1) at discharge from initial hospitalization and (2) 18 to 24 months postnatal age was examined. RESULTS: Compared with survivors, the nonsurvivors had higher lactate concentrations on admission to the pediatric intensive care unit at day 1 peak and area under the curve of the lactate profile than those of adverse and intact survivors (all P < .001, analysis of variance). Significant differences in the time for lactate concentrations to return to 2 mmol/L or less during the first postoperative day were observed among the groups: nonsurvivors > adverse survivors > intact survivors. Lactate concentrations of less than 7 mmol/L on admission or less than 8 mmol/L at day 1 peak predicted survival with 82% sensitivity and 83% specificity, and positive and negative predictive values of 97% and 43%, respectively (P < .001, chi2). Plasma lactate concentrations were associated with adverse outcome but had lower predictive values compared with that for nonsurvival. CONCLUSIONS: Serial lactate determination accurately predicts survival and may help differentiate survivors with adverse outcome from those with intact neurodevelopment in early childhood.

Biomarkers↗
PubMed2005

The role of lactate in brain metabolism.

According to the astrocyte-neurone-lactate shuttle (ANLS) hypothesis, activated neurones use lactate released by astrocytes as their energy substrate. The hypothesis, based largely on in vitro experiments, postulates that lactate is derived from the uptake by astrocytes of synaptically released glutamate. The time course of changes in lactate, derived from in vivo experiments, is incompatible with the ANLS model. Neuronal activation leads to a delayed rise in lactate followed by a slow decay, which greatly outlasts the period of neuronal activation. The present review proposes that the uptake of stimulated glutamate release from astrocytes, rather than synaptically released glutamate, is the source of lactate released following neuronal activation. This rise in lactate occurs too late to provide energy for neuronal activity. Furthermore, there is no evidence that lactate undergoes local oxidative phosphorylation. In conclusion, under physiological conditions, there is no evidence that lactate is a significant source of energy for activated neurones.

Animals↗
PubMed2005

Lactate production by thrombin-activated platelets of patients with primary thrombocythemia.

INTRODUCTION: Platelet activation needs a high energy demand which is supplied by the degradation of glucose into lactate. Platelet response to agonists in patients with primary thrombocythemia is defective. We studied the production of lactate by the platelets of patients with this disease and defective platelet aggregation. MATERIAL AND METHODS: Ten patients suffering from primary thrombocythemia and ten controls were included in this study. The lactate generation was measured in resting and thrombin activated platelets in absence or presence of glucose. RESULTS: Resting platelets incubated for 30 min in phosphate-buffered saline (PBS) generated the same amount of lactate in patients (44.6+/-21.6 micromol/10(11) cells) and controls (41.0+/-17.3 micromol/10(11) cells). Addition of glucose led to similar increases in lactate formation by platelets in patients (82.2+/-26.4 micromol/10(11) cells) and controls (88.1+/-34.5 micromol/10(11) cells). The addition of thrombin in absence of glucose did not modify the lactate formation respective to PBS. Finally, the incubation of platelets with both glucose and thrombin caused further increases in the generation of lactate in both groups, patients (236.9+/-83.9 micromol/10(11) cells) and controls (228.6+/-63.5 micromol/10(11) cells) without differences between them. The production of lactate in both groups was also similar when platelets were incubated for 10 min or 20 min with both thrombin and glucose. However at 5 min, platelets of patients generated more lactate (97.8+/-23.7 micromol/10(11) cells) than controls (66.5+/-38.7 micromol/10(11) cells, p<0.05). CONCLUSIONS: These results suggest that thrombin is able to induce an initial hyperactivity of those pathways involved in the platelet energy production of patients with primary thrombocythemia.

Adolescent↗
PubMed2001

Comparison of glucose and lactate as substrates during NMDA-induced activation of hippocampal slices.

It has been postulated that lactate released from astrocytes may be the preferred metabolic substrate for neurons, particularly during intense neuronal activity (the astrocyte-neuron lactate shuttle hypothesis). We examined this hypothesis by exposing rat hippocampal slices to artificial cerebrospinal fluid containing either glucose or lactate and either N-methyl-D-aspartate, which activates neurons without stimulating astrocytic glucose uptake, or alpha-cyano-4-hydroxycinnamate, which blocks monocarboxylate transport across plasma and mitochondrial membranes. When exposed to N-methyl-D-aspartate, slices lost synaptic transmission and K+ homeostasis more slowly in glucose-containing artificial cerebrospinal fluid than in lactate-containing artificial cerebrospinal fluid. After N-methyl-D-aspartate exposure, slices recovered synaptic transmission more completely in glucose. These results suggest that hippocampal neurons can use glucose more effectively than lactate when energy demand is high. In experiments with alpha-cyano-4-hydroxycinnamate, 500 microM alpha-cyano-4-hydroxycinnamate caused loss of K+ homeostasis and synaptic transmission in hippocampal slices during normoxia. When 200 microM alpha-cyano-4-hydroxycinnamate was used, synaptic activity and intracellular pH in slices decreased significantly during normoxia. These results suggest that alpha-cyano-4-hydroxycinnamate may have blocked mitochondrial oxidative metabolism along with lactate transport. Thus, studies using alpha-cyano-4-hydroxycinnamate to demonstrate the presence of a lactate shuttle in the brain tissue may need reevaluation. Our findings, together with observations in the literature that (1) glucose is available to neurons during activation, (2) heightened energy demand rapidly activates glycolysis in neurons, and (3) activation of glycolysis suppresses lactate utilization, suggests that glucose is the primary substrate for neurons during neuronal activation and do not support the astrocyte-neuron lactate shuttle hypothesis.

Animals↗
PubMed1999

Leukocyte glycolysis and lactate output in animal sepsis and ex vivo human blood.

Lactate is released in large quantity from sites of sepsis and inflammation. We asked whether the increased lactate production found in sepsis can be explained by the augmented glycolysis of inflammatory cells. The glycolytic metabolism of rat peritoneal leukocytes was measured following cecal ligation and perforation (CLP) or sham laparotomy. CLP augmented glucose uptake, the pentose phosphate pathway, and glucose oxidation. Lactate output increased from 1.03 +/- 0.05 to 1.20 +/- 0.05 fmol x cell(-1) x min(-1) (P < .001). Total lactate output of peritoneal lavage fluid increased from 7.94 +/- 2.59 to 28.12 +/- 5.60 nmol L x min(-1) (P < .005). The effect of lipopolysaccharide (LPS) on the lactate output of whole blood from 31 critically ill patients was measured. Leukocyte lactate production was calculated by multiple linear regression analysis. Following exposure to LPS, human leukocyte lactate output increased from 0.20 +/- 0.09 to 1.22 +/- 0.14 fmol x cell(-1) x min(-1) (P < .001). This rate of production is so high that it suggests that the lactate output of different tissue beds in sepsis may be affected by their different cell populations and state of activation. This study supports the hypothesis that lactate may be more a product of inflammation than a marker of tissue hypoxia in sepsis.

Animals↗
PubMedDate not supplied

Glucose and lactate turnover in adults with falciparum malaria: effect of complications and antimalarial therapy.

Hypoglycaemia and lactic acidosis are potentially life-threatening, poorly understood sequelae of Plasmodium falciparum infections. We investigated relationships between clinical status, treatment, and glucose and lactate kinetics during management of falciparum malaria in 14 Vietnamese adults. Nine had severe malaria, of whom 4 were administered quinine (Group 1a) and 5 artesunate (Group 1b). Five uncomplicated cases received artesunate (Group 2). Glucose and lactate turnover were studied on 3 occasions: (i) immediately after initial antimalarial treatment, (ii) at parasite clearance a median of 3 days later, and (iii) at discharge from hospital a median of 9 days post-admission. Steady-state glucose and lactate kinetics were derived from plasma isotopic enrichment during a primed-continuous infusion of D-[6,6-D2]glucose and a parallel infusion of L-[1-13C]lactate. Group 1a patients had the lowest plasma glucose concentrations in the admission study (median [range] 3.9 [3.6-5.1] vs 6.3 [4.9-7.1] and 4.5 [4.3-5.5] mmol/L in Groups 1b and 2 respectively; P < 0.05 vs Group 1b), but glucose production rates and serum insulin concentrations that were similar to those in the other groups (P > 0.17). This was also the case at parasite clearance and suggested an inappropriate beta cell response. Group 1a patients had the highest admission lactate production (60 [36-77] vs 26 [21-47] and 22 [4-31] mumol/kg.min in Group 1b and 2 respectively; P < 0.05 vs Group 2). Amongst the 9 severe cases, there was an inverse association between plasma glucose and lactate production at admission and parasite clearance (P < 0.05), but no correlation between admission lactate production and serum bicarbonate (P = 0.73). The present data confirm previous studies showing that quinine depresses plasma glucose through stimulation of insulin secretion. It is hypothesized that the low plasma glucose activates Na+,K(+)-ATPase through increased plasma catecholamine concentrations, leading to accelerated glycolysis and increased lactate production in well-oxygenated tissues. In some severely ill patients with falciparum malaria, a raised plasma lactate on its own may, therefore, be an unreliable index of a developing acidosis.

Adolescent↗
PubMed2001

Comparison of lactate or BE during out-of-hospital cardiac arrest to determine metabolic acidosis.

During cardiopulmonary resuscitation, pH and base excess (BE) decrease to a variable degree due to metabolic acidosis. The main cause has been shown to be lactate, which cannot be eliminated sufficiently because of low perfusion during cardiac massage. Both BE and lactate can be measured in the prehospital phase. The aim of the study was to determine if BE and lactate are comparable variables during cardiopulmonary resuscitation (CPR) and if the measurement of lactate level alone would be sufficient to determine the patient's metabolic status and sufficiently reliable to determine the administration of buffer solutions. During the observation period, we registered 31 patients (21 males, ten females) who were resuscitated according to European Resuscitation Council recommendations, who had blood gas analysis and lactate levels measured in blood taken by arterial puncture or arterial line. The first measurement from each patient was taken after primary resuscitation (within 5-20 min). The mean lactate level was 9.85+/-2.98 (range, 4.1-18.7) mmol/l, and the mean BE was -15.0+/-5.98 (range, 5.5 to -24.3). There were statistically significant correlations between the lactate level and BE and pH (linear correlation, r=-0.673, P<0,001 and r=-0,683, P<0,001, respectively), but not with pO2 and pCO2. The receiver-operated curve analysis showed that a cut-off point of 7.0 mmol/l lactate indicates a BE below -10 with a sensitivity of 96% and a specificity of 67%. Lactate measurement is a valuable tool to determine metabolic acidosis during CPR and may be able to replace blood gas analysis in this situation.

Acidosis↗
PubMed2001

Udder disease etiology, milk somatic cell counts and NAGase activity in Israeli Assaf sheep throughout lactation.

Bacterial pathogens causing udder infections in Israeli Assaf dairy sheep were identified and changes occurring throughout lactation were monitored to study the correlation between the contaminant and the severity of the infection, as measured by somatic cell count (SCC) and NAGase tests. A total of 159 Israeli Assaf dairy sheep on one farm, in their first (69), second (13) or third and more (77) lactations were included in this study. Udder halves were tested for bacterial condition, SCC and NAGase activity 2-3 weeks post lambing and every 4 weeks after until drying-off. At first sampling, in 60.7% (193/318 quarters) of the halves no bacterial growth (NBG) was detected. Different species of coagulase negative staphylococci (CNS) were the main pathogen group in infected udders. Streptococci were isolated from 14 halves, most of them in the two udder halves. The percent of udder infection in sheep in their third or further lactations was 2.8 greater (P<0.05) than in that of sheep in their first lactation. During the lactation, 90.6% of the halves did not change their classification status, suggesting that most infections occur before lambing and/or during the following first few days. The arithmetic mean of SCC and NAGase of total half udder milk and samplings (during the lactation) were 1144+/-48x10(3)cells/ml and 49.4+/-2.5, respectively. The average SCC in the milk of halves classified as NBG was 321+/-35x10(3)cells/ml and was not significantly changed during the lactation period. In halves infected with CNS, average SCC was 1371+/-150x10(3)cells/ml at the first testing and increased to 2129+/-347x10(3)cells/ml at drying-off. No significant differences were found in SCC and NAGase activity between the different species of the CNS. The mean SCC over the types of bacteria isolated, lactation number and days in lactation was significantly different (P<0.0001). In 4% of the halves, from all samples, SCC was above 5000x10(3)cells/ml although no bacteria were detected in their milk. The higher SCC in the CNS infected halves contrasted with the more moderate SCC found in dairy cows similarly infected, suggesting that the sheep udder has a lower resistance and an augmented immunological response against this group of bacteria. Thus, this should be considered accordingly in schemes for sheep's milk quality payment.

Journal Article↗
PubMedDate not supplied

Effects of ammonium and lactate on growth and metabolism of a recombinant Chinese hamster ovary cell culture.

A Chinese hamster ovary (CHO) cell line producing a recombinant glycoprotein was cultured in batch mode with different initial concentrations of ammonium chloride (0-10 mM), sodium lactate (0-60 mM), or sodium chloride (0-60 mM). High ammonium concentrations did not inhibit cell growth and productivity or glucose and glutamine consumption. In contrast, specific ammonia and alanine production decreased by 55% and 40%, respectively. There were also significant increases in specific aspartate and glutamate consumption in high ammonium concentrations. These observations indicated a shift in glutamine catabolic pathways in response to the effects of ammonium. The influence of lactate on growth and metabolism were the combined effects of lactate concentration and osmolarity. After "correcting" for osmolarity effects, lactate was found to inhibit growth by 25% but to increase specific productivity slightly (10%). Lactate had profound effects not only on glycolysis but also on glutaminolysis. While specific glucose and glutamine consumptions decreased by 15-20%, the effects of lactate on their metabolic products were far more significant. Lactate production was halted, and specific ammonia and alanine productions decreased by 64% and 70% at high lactate concentration. Theories on how ammonium and lactate affected the metabolic pathways of glucose and glutamine are presented.

Ammonium Chloride↗
PubMed2001

Increased lactate production follows loss of mitochondrial membrane potential during apoptosis of human leukaemia cells.

Acute tumour-lysis syndrome (ATLS) is a frequently fatal complication after cytoreductive leukaemia therapy. Lactic acidosis is associated with ATLS and its extent is correlated with the severity of ATLS. In the course of cytoreductive therapy, apoptosis is induced in tumour cells, which results in loss of mitochondrial function. We hypothesize that loss of mitochondrial function leads to compensatory glycolysis, which is the main cause of lactate accumulation and acidosis. We tested this hypothesis using the model of glucocorticoid-induced apoptosis in the human acute lymphoblastic leukaemia cell line CCRF-CEM. After induction of glucocorticoid-induced apoptosis, a biphasic course of lactate production was observed. Prior to the onset of apoptosis, i.e. prior to the loss of membrane potential, lactate production was reduced. However, subsequent to loss of mitochondrial membrane potential a massive increase in lactate production was observed (15.5 +/- 0.5 versus 10.17 +/- 0.09 mmol/10(6) cells, P = 0.001). We also demonstrated that inhibition of respiratory chain activity by antimycin A resulted in excess lactate production. In the model cell line used, conditional bcl-2 expression delayed glucocorticoid-induced apoptosis by protecting against loss of mitochondrial membrane potential; bcl-2 expression delayed the increase in lactate production and had no effect on the pre-apoptotic drop in lactate production. Apoptosis-induced lactate production was also observed in other cell lines (HL60, THP1 and OPM2) with various cytotoxic agents [doxorubicin, gemcitabine and vumon (VM26)]. Thus, the data suggest that lactate acidosis can be caused by apoptotic loss of mitochondrial function and massive apoptosis of a tumour mass via lactic acidosis may be the essential pathological event in ATLS.

Antineoplastic Agents, Hormonal↗
PubMed2002

Lactate in the brain of the freely moving rat: voltammetric monitoring of the changes related to the sleep-wake states.

Cortical lactate was monitored voltammetrically in freely moving rats equipped with polygraphic electrodes. Differential normal pulse voltammetric measurements were carried out using a lactate biosensor coated with lactate oxidase and cellulose acetate. Changes occurring in lactate level were in keeping with sleep-wake states. During slow wave sleep (SWS), the lactate level decreased significantly (-16.2%) vs. the spontaneous waking state (W) referenced to as 100%. During paradoxical sleep (PS), and still vs. W, it remained low (-9.0%) but this variation was not statistically significant. However, when this PS change was compared to the SWS variation, a significant increase in lactate level was then revealed (+8.5%). Finally, during the active waking (aW) triggered by a water puff stress, lactate level rose significantly in accordance with the animal activity (+53% compared to W). Long-term monitoring also allowed the determination of a circadian component in lactate production, the lowest and highest values being monitored during light and dark periods, respectively. The acrophasis of the circadian change occurred during the dark period, about 3 h after the light-off (+89%). It is suggested that during wakefulness astrocyte metabolism allows the transformation of the blood-borne glucose into lactate. The increase in this substrate observed during PS may fulfil the oxidative phosphorylation in order to supply the important ATP need of PS.

Animals↗
PubMed2001

Streptozotocin-induced diabetes decreases rat sarcolemmal lactate transport.

Impaired lactate metabolism is a metabolic disorder, which is not fully understood in the diabetic state including streptozotocin (STZ)-induced diabetes. We investigated whether STZ-induced diabetes results in altered lactate exchanges using the rat muscle sarcolemmal vesicles (SV) model. Fifteen days after diabetes onset (1 STZ-injection, 65 mg/kg, intraperitoneal [IP]), rats had higher blood and muscle lactate concentrations compared with normal rats (1.50 +/- 0.09 v 1.95 +/- 0.21 mmol/L (not significant [NS]) and 21.02 +/- 1.26 v 25.53 +/- 0.98 mmol/kg wet weight (ww); P < .05). The initial rate of lactate uptake was measured at various external lactate concentrations using SV of both group in zero-trans conditions. STZ-induced diabetes decreased the initial rate of total lactate influx at external lactate concentrations from 1 to 100 mmol/L (P < .05). This decrease in lactate transport was found in addition to an increased free radical production, as indicated by a significant increase in malonedialdehyde (MDA) concentration (64.3 +/- 8.7 v 100.3 +/- 13.5 nmol. g(-1) ww, P < .05), coupled with a higher glutathione peroxidase (Gpx) activity (48.03 +/- 3.13 v 84.7 +/- 15.01 micromol. min(-1). mg(-1) protein, P < .05) in red gastrocnemius. We concluded that STZ-induced diabetes decreases total lactate transport activity in rat SV and is associated with increased muscular oxidative stress.

Animals↗
PubMed2000

Increase characteristics of the cumulated excess-CO2 and the lactate concentration during exercise.

The so-called excess-CO2 in physical exertion results stoichiometrically directly from the quantity of protons bound in bicarbonate buffering. This situation is used in determining the ventilatory threshold (VT). However, the extent to which the degree and increase characteristics of excess-CO2 can be used as an equivalent to blood lactate concentrations is uncertain. To investigate this relationship, 21 healthy men exercised on a cycle ergometer (starting at 50 watt, increases of 50 watt every 3 minutes) to subjective exhaustion. To evaluate the characteristics of this increase, a slope constant lambda was calculated in relation to performance for both the blood lactate concentration (lambda lactate) and the cumulated excess-CO2 (lambda CO2 excess). The start of the lactate increase (LT) and excess-CO2 (VT) showed good intercorrelation (VT=2.27+0.98 x LT; r=0.914; P<0.001). Mean lambda lactate and lambda CO2 excess were of similar dimensions in all subjects (69.3 +/- 39.8 watt vs. 80.11 +/- 15.7 watt), but a minority of the subjects (n=7) showed a considerably more gradual increase for the excess-CO2 to the maximum. Since in addition there was no significant correlation between the absolute values for maximum lactate concentrations and the cumulative excess-CO2, an interindividual prediction of lactate concentrations from the excess-CO2 would be difficult. It is an open question, however, whether perhaps additional performance-limiting factors, such as the ventilation or the buffering capacity, may be included when measuring the excess-CO2 so that this parameter could be more a measure for the formation rate of new lactate than the blood lactate concentration alone.

Adult↗
PubMed2001

Lactate is correlated with the indocyanine green elimination rate in liver resection for cirrhotic patients.

UNLABELLED: The role of lactate in liver ischemia-reperfusion injury in cirrhosis has not been clarified. Fifty patients with hepatocellular carcinoma who underwent partial liver resection under Pringle's maneuver were included in this study. We performed the indocyanine green clearance test before the operation and three times during the surgery to calculate its elimination rate. Blood lactate and base excess were measured at the corresponding times. Systolic and diastolic systemic arterial pressure, heart rate, cardiac index, and esophageal temperature were monitored. Aminotransferase levels were recorded the day before the operation, 1 h after the operation, and on the first and third postoperative days. We calculated the increase or decrease in lactate levels during the preischemic, ischemic, and postischemic phases, and examined the correlation between these results and the changes in indocyanine green elimination rate and some clinical factors. The lactate levels increased before reperfusion and began to decrease after reperfusion. The lactate increase and decrease during the ischemic and postischemic phases correlated with the change in indocyanine green elimination rate (P < 0.0001 and P = 0.02 for the respective phases). The lactate increase during the preischemic phase correlated with the duration of the preischemic phase (P < 0.0001). In cirrhotic patients who undergo liver resection with Pringle's maneuver and who do not show postoperative liver failure, the blood lactate profile might be a reliable indicator of liver metabolic capacity during surgery. IMPLICATIONS: In cirrhotic patients who underwent liver resection with Pringle's maneuver, the lactate increase and decrease during the ischemic and postischemic phases correlated with the change in the indocyanine green elimination rate. The blood lactate profile might be a reliable indicator of liver metabolic capacity during surgery.

Adult↗
PubMed2002

Intravenous L-lactate application in minipigs partially protects acetylcholinesteratic but not butyrylcholinesteratic activity in plasma from inhibition by paraoxon.

OBJECTIVE: Intoxications with organophosphorous compounds such as paraoxon, an inhibitor of serine hydrolases, mainly butyrylcholinesterase and acetylcholinesterase, are frequent. Oximes are the only enzyme reactivators clinically available. In vitro studies have shown that L(+)-lactate reduces the inhibition of acetylcholinesteratic (AChEA) and butyrylcholinesteratic activity of plasma (BChEA) by paraoxon. DESIGN: The purpose of this in vivo study was to determine whether intravenous L(+)-lactate application under normoxic/normocapnic/normohydrogenemic conditions is able to protect AChEA and BChEA from paraoxon inhibition. SETTING: University research institute. SUBJECTS: Eighteen female minipigs. INTERVENTIONS: Animals were anesthetized, intubated, and mechanically ventilated. Every animal received 1 mg of paraoxon per kilogram of body weight in 50 mL of saline over 50 mins. In addition to receiving paraoxon, six pigs of 18 received 2.5 g (0.125 g kg-1 of body weight) of intravenous L(+)-lactate in 50 mL of saline over 50 mins, and six other pigs received 10 g of L(+)-lactate (0.5 g kg-1 of body weight), whereas the six remaining served as controls. MEASUREMENTS AND MAIN RESULTS: In central venous blood, plasma acetylcholinesteratic and butyrylcholinesteratic activity were measured before paraoxon (baseline, 0 mins), immediately after paraoxon (50 mins after start), and 110, 170, 230, 290, 530, and 1010 mins after the start of infusion. Although 10 g of intravenous L(+)-lactate application had a statistically significant protective effect in vivo on AChEA, 2.5 g did not. No significant protective effect on BChEA was achieved with either 2.5 g or 10 g of L(+)-lactate. CONCLUSIONS: Ten grams of L(+)-lactate can increase AChEA when administered simultaneously with paraoxon. Further study of the in vivo effects of L(+)-lactate after paraoxon intoxication and a formal comparison with standard oxime therapy seem warranted. Also, methods for achieving a prolonged elevated lactate concentration in vivo should be investigated.

Acetylcholinesterase↗
PubMed2000

Cerebral metabolism of lactate in vivo: evidence for neuronal pyruvate carboxylation.

The cerebral metabolism of lactate was investigated. Awake mice received [3-13C]lactate or [1-13C]glucose intravenously, and brain and blood extracts were analyzed by 13C nuclear magnetic resonance spectroscopy. The cerebral uptake and metabolism of [3-13C]lactate was 50% that of [1-13C]glucose. [3-13C]Lactate was almost exclusively metabolized by neurons and hardly at all by glia, as revealed by the 13C labeling of glutamate, gamma-aminobutyric acid and glutamine. Injection of [3-13C]lactate led to extensive formation of [2-13C]lactate, which was not seen with [1-13C]glucose, nor has it been seen in previous studies with [2-13C]acetate. This formation probably reflected reversible carboxylation of [3-13C]pyruvate to malate and equilibration with fumarate, because inhibition of succinate dehydrogenase with nitropropionic acid did not block it. Of the [3-13C]lactate that reached the brain, 20% underwent this reaction, which probably involved neuronal mitochondrial malic enzyme. The activities of mitochondrial malic enzyme, fumarase, and lactate dehydrogenase were high enough to account for the formation of [2-13C]lactate in neurons. Neuronal pyruvate carboxylation was confirmed by the higher specific activity of glutamate than of glutamine after intrastriatal injection of [1-14C]pyruvate into anesthetized mice. This procedure also demonstrated equilibration of malate, formed through pyruvate carboxylation, with fumarate. The demonstration of neuronal pyruvate carboxylation demands reconsideration of the metabolic interrelationship between neurons and glia.

Animals↗