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PubMed1997

Dissociation between lactate and proton exchange in muscle during intense exercise in man.

1. Transport of lactate, H+ and fluid across muscle sarcolemma was studied in contracting muscles under varying blood acid-base conditions. 2. Subjects performed two-legged submaximal knee-extensor exercise for 29-35 min consisting of warming up for 5 min followed by 10 min of leg exercise (L1), leg and arm exercise for 6-10 min (L2 + A) and leg exercise for 10 min (L3). The experimental protocol was performed on two occasions; inspiring air (normoxia, N) or breathing 14% O2 in N2 (hypoxia, H). Leg blood flow was measured and femoral arterial and venous blood was sampled before and during each phase of exercise. 3. Arterial blood lactate concentration increased progressively during exercise to 5.9 +/- 0.8 (N) and 8.2 +/- 0.8 mmol l-1 (H) (P < 0.05) after 5.5 min of L2 + A. Arterial blood pH was higher (P < 0.05) in H than in N, whereas arterial blood HCO3- concentrations were the same. Leg lactate release was higher in H than in N (3.1 +/- 0.7 vs. 2.0 mmol l-1 (P < 0.05) during L1. In L2 + A a net uptake of lactate was observed in both N and H. The concentration of lactate in the red blood cells increased during exercise to 2.3 +/- 0.4 (N) and 4.3 +/- 0.7 mmol l-1 (H) (P < 0.05) after 5.5 min of L2 + A, but no red blood cell femoral arterial-venous lactate difference was observed. 4. Net proton release, estimated from actual base excess (ABE) adjusted for changes in reduced haemoglobin, was significant (P < 0.05) both at rest and during each phase of exercise. Furthermore, the difference between net proton and lactate release was positive throughout exercise and of similar magnitude in N and H. 5. The present data suggest that (1) H+ exchange in muscle during submaximal exercise can to a large extent occur through mechanisms other than via coupling to lactate; (2) muscle transport of H+ is insensitive to changes in blood pH in the range of 0.02-0.08 pH units; (3) transport of lactate across the membrane of red blood cells appears to be of minor importance for lactate release from active muscles.

Acid-Base Equilibrium↗

PubMed1998

Lactate compared with pH analysis at fetal scalp blood sampling: a prospective randomised study.

OBJECTIVE: Fetal scalp blood sampling is a widely used method for assessing fetal condition in the event of ominous fetal heart rate patterns. The purpose of this randomised trial was to compare the value of fetal scalp blood lactate and pH management in cases of abnormal intrapartum fetal heart rate tracings. METHODS: Of 341 cases of ominous fetal heart rate patterns, 169 were randomly assigned to pH analysis, and 172 to lactate measurements. Lactate was measured using a lactate card requiring 5 microL of blood and yielding the result within 60 seconds. pH analysis was performed with an ABL 510 acid-base analyser requiring 35 microL of blood and yielding the results within 47 seconds. RESULTS: Unsuccessful fetal blood sampling procedures (no result or an unreliable result) occurred significantly more often in the pH subgroup than in the lactate subgroup (OR 16.1 with 95% CI 5.8-44.7). In the pH subgroup the failure rate was inversely related to the degree of cervical dilatation. Compared with the pH subgroup, the lactate subgroup was characterised by fewer fetal scalp incisions per blood sampling attempt (median 1.0 [interquartile range (IQR) 1-1] vs 2.0 [IQR 1-2]), and significantly less time required for the sampling procedure (median 120 s [IQR 90-147] vs 230 s [IQR 180-300]). The groups did not differ in mode of delivery, neonatal outcome and umbilical artery acid-base balance and lactate levels. CONCLUSION: This trial showed the levels of lactate and pH in fetal scalp blood to be comparable in predicting perinatal outcome, but the procedure to measuring lactate was more successful than that for pH. Owing to its simplicity of performance, lactate analysis is an attractive alternative for intrapartum fetal monitoring.

Female↗

PubMed1998

Lactate causes changes in gonococci including increased lipopolysaccharide synthesis during short-term incubation in media containing glucose.

Gonococci (strain BS4(agar)), emerging from lag-phase during 1-1.5 h incubation in a medium containing glucose (28 mM) and either 5 microM or 50 microM sodium lactate, show enhanced capacity for their lipopolysaccharide (LPS) to be sialylated by cytidine 5'-monophospho-N-acetyl neuraminic acid. The sialyltransferase content of the lactate-treated gonococci was not greater than that of control organisms and showed no differences in LPS components. However, the total LPS content of the lactate-treated gonococci was 10-20% higher than that of control organisms, so lactate enhancement may be due to more sialyl receptors becoming available due to an overall stimulation of LPS synthesis. The protein and pentose contents of the lactate-treated gonococci were also higher than those of controls, indicating stimulation of protein synthesis and ribosome production. Electron microscopy showed hair-like external appendages on control but not on lactate-treated gonococci. The above growth conditions are unnatural. However, when concentrations of glucose and lactate were adjusted to values akin to those occurring in vivo (glucose 5 mM alone and with either 1 mM or 10 mM lactate), and gonococcal multiplication occurred during the short incubation period (1-1.5 h), lactate again induced greater contents of LPS, protein and pentose. A high content of LPS, which will contribute to pathogenicity, should be a constant feature of gonococci growing in human urogenital tissues, where lactate is ever present with glucose.

Bacterial Proteins↗

PubMed1997

Stimulated release of lactate in freely moving rats is dependent on the uptake of glutamate.

1. Physiological stimulation of neuronal activity induces an increase in extracellular lactate. Experiments were designed to determine the role of the reuptake of neuronally released glutamate in lactate delivery to the extracellular compartment. 2. In vivo microdialysis was used in freely moving rats. The lactate concentration in striatal dialysate was assayed using an enzyme-based on-line assay at 1 min intervals. Drugs were given locally through the dialysis probe. 3. The extracellular concentration of lactate, determined using the zero net flux method, was 346 +/- 21 microM. 4. Induced grooming caused a maximal increase in lactate concentration in striatal dialysate of 58 +/- 10%. 5. Administration of 100 microM glutamate caused a transient increase in dialysate lactate concentration of 72 +/- 17%. 6. A 20 min infusion of the glutamate uptake blockers beta-D,L-threohydroxyaspartate (THA) or pirrolidine-2-4-dicarboxylate (PDC) produced an increase in basal lactate, which was sustained in response to THA and transient in response to PDC. 7. Grooming induced during the infusion of PDC produced no significant increase in lactate. 8. Grooming induced after the infusion of the glutamate uptake blockers gave rise to a reduced increase in lactate. 9. These results support the hypothesis that stimulated release of lactate is dependent on the uptake of glutamate.

Amino Acid Transport System X-AG↗

PubMed1996

A new approach to the assessment of anaerobic metabolism: measurement of lactate in saliva.

OBJECTIVE: To test the hypothesis that saliva lactate concentrations may reflect those present in blood and that saliva lactate can be used as a very convenient and useful variable in the study of anaerobic metabolism. METHODS: Parallel determinations were made of lactate in saliva and in capillary blood samples, obtained at 3 min intervals from nine individuals during the performance of a maximum graded exercise test on a cycle ergometer against increasing workloads (from 25 up to a maximum of 300 W). Lactate determinations were done by means of an electroenzymatic method using 25 microliters samples in both types of fluids. RESULTS: For each situation, the concentration of lactate in saliva was shown to be about 15% of that in plasma but it followed the same pattern of evolution during the exercise test. A good correlation (r = 0.81) between blood and saliva lactate concentrations was found. The precision of the method was very good, with a coefficient of variation ranging (n = 10) between 2.2% for samples with very low lactate concentrations and 0.7% for sample with moderate lactate concentrations. Lactate appeared to be very stable in saliva over a period of 40 days after collection, when kept at 4 degrees C. The values obtained after this period were virtually identical to those shown in fresh samples. CONCLUSIONS: Determination of lactate in saliva can be used as an alternative to determination in blood, overcoming most of the drawbacks of the procedures being used at present, since the collection of the samples required no special expertise.

Adult↗

PubMed2006

Lactate release from adipose tissue and skeletal muscle in vivo: defective insulin regulation in insulin-resistant obese women.

To study the local tissue lactate production in the normal state and its possible disturbances in insulin resistance, rates of lactate release from adipose tissue (AT) and skeletal muscle (SM) were compared postabsorptively and during a hyperinsulinemic euglycemic clamp in 11 healthy nonobese and 11 insulin-resistant obese women. A combination of microdialysis, to measure interstitial lactate, and the 133Xe clearance technique, to determine local blood flow, were used. In the controls, local blood flow increased by 40% in SM (P<0.05) and remained unchanged in AT, whereas the interstitial-plasma difference in lactate doubled in AT (P<0.005) and was unaffected in SM during hyperinsulinemia. In the obese, blood flow and interstitial-plasma difference in lactate remained unchanged in both tissues during hyperinsulinemia. The lactate release (micromol100 g-1min-1) was 1.17+/-0.22 in SM and 0.43+/-0.11 in AT among the controls (P<0.01) and 0.86+/-0.23 in SM and 0.83+/-0.25 in AT among the obese women in the postabsorptive state. During insulin infusion, lactate release in the controls increased to 1.92+/-0.26 in SM (P<0.005) and to 1.14+/-0.22 in AT (P<0.005) but remained unchanged in the obese women. It is concluded that AT and SM are both significant sources of lactate release postabsorptively, and AT is at least as responsive to insulin as SM. The ability to increase lactate release in response to insulin is impaired in AT and SM in insulin-resistant obese women, involving defective insulin regulation of both tissue lactate metabolism and local blood flow.

Adipose Tissue↗

PubMed2001

Lactate-transport activity in RBCs of trained and untrained individuals from four racing species.

In red blood cells (RBC) of horses, both lactate-transport activity and lactate accumulation during races vary interindividually. To study whether similar variation in lactate transport is apparent also in RBCs of other racing species, blood samples were collected from 21 reindeer, 40 horses, 31 humans, and 38 dogs. Total lactate-transport activity was measured at 10 and 30 mM concentrations, and the roles of the monocarboxylate-transporter (MCT) and the inorganic anion-exchange transporter (band-3 protein) were studied with inhibitors. In the reindeer and in one-third of the horses, lactate transport was low and mediated mainly by band-3 protein and nonionic diffusion. In the humans, dogs, and the remaining two-thirds of the horses, lactate transport was high and MCT was the main transporter. No correlation existed between MCT activity and the athleticism of the species. In the horses and humans, training had no effect on lactate transport, but in the reindeer and sled dogs, training increased total lactate transport. These results show that among the racing species studied, only in horses was the distribution of lactate-transport activity bimodal, and the possible connection between RBC lactate and performance capacity, especially in this species, warrants further studies.

4,4'-Diisothiocyanostilbene-2,2'-Disulfonic Acid↗

PubMed1997

Lactate production by the lungs in acute lung injury.

Arteriovenous differences in lactate (AVLAC) across the lungs are usually small and close to zero. However, it has recently been reported that the lungs can produce increased amounts of lactate in some patients with acute respiratory distress syndrome (ARDS). The aim of this study was to evaluate lactate production in various types of acute lung injury requiring mechanical ventilation and hemodynamic monitoring. Since the differences involved are usually small, minor errors in lactate measurement could greatly influence AVLAC. Based on an analysis of these errors (see text for details), we averaged five arterial and venous samples for each measurement. We investigated 122 patients: 43 with acute lung injury (ALI), nine with cardiogenic pulmonary edema (CPE), 37 with bronchopneumonia (BPN), seven with single lung transplantation (LTX), and 26 with other causes of respiratory failure (OTHER). There was no difference in arterial lactate between the various groups. AVLAC was higher in patients with ALI than in the other groups (0.20+/-0.23 versus 0.07+/-0.11 mEq/L). In patients with ALI, AVLAC was proportional to the Murray's lung injury score (-0.032+/-0.032x; r = 0.46, p < 0.01). Lung lactate production was calculated as the product of the cardiac index times AVLAC and was significantly higher in patients with ALI than in the other groups (0.69+/-0.88 versus 0.19+/-0.30 mEq/min; p < 0.05). In patients with ALI, lung lactate production was inversely related to the PaO2/FIO2 (1.42 - 0.005x; r = 0.35, p < 0.05) but directly related to the venous admixture (-0.36 + 0.003x; r = 0.49, p < 0.01) and the lung injury score (-0.19 + 0.36x; r = 0.45, p < 0.01). Lung lactate production was not significantly related to arterial lactate levels. These data indicate that AVLAC and lung lactate production can be increased in patients with ARDS but remain within the normal range in other types of respiratory failure.

Acute Disease↗

PubMed2006

Dilation of retinal arterioles in response to lactate: role of nitric oxide, guanylyl cyclase, and ATP-sensitive potassium channels.

PURPOSE: Lactate, a key metabolite in the retinal tissue, has been implicated in regulating retinal blood flow to match retinal metabolic demand. However, the direct effect of lactate on retinal vascular tone and the possible underlying signaling mechanisms remain unknown. In the present study, the roles of endothelium-derived vasodilators, guanylyl cyclase, and potassium channels were examined in lactate-induced dilation of retinal arterioles in vitro. METHODS: Porcine second-order retinal arterioles were isolated, cannulated, and pressurized to 55 cm H2O lumenal pressure without flow. Diameter changes in response to agonists were recorded with videomicroscopic techniques. RESULTS: All vessels developed basal tone (approximately 70 microm in internal diameter) and dilated dose dependently in response to neutralized L-lactate (0.01-10 mM). Inhibition of cyclooxygenase by indomethacin only slightly reduced the vasodilatory response to lactate. In contrast, blockade of monocarboxylate transporters, nitric oxide (NO) synthase, soluble guanylyl cyclase, and ATP-sensitive potassium (KATP) channels nearly abolished lactate-induced vasodilation. The cGMP phosphodiesterase inhibitor zaprinast enhanced the vasodilation response to lactate. Similar to the lactate-induced response, the vasodilation elicited by S-nitroso-N-acetylpenicillamine, an NO donor that activates cGMP signaling, was also inhibited by the soluble guanylyl cyclase and KATP channel blockers. CONCLUSIONS: These data suggest that uptake of lactate by vascular cells via monocarboxylate transporters causes retinal arteriolar dilation predominantly via stimulation of NO synthase and subsequent activation of guanylyl cyclase. The guanylyl cyclase/cGMP signaling triggers opening of KATP channels for vasodilation. A better understanding of the fundamental signaling pathways responsible for lactate-induced dilation of retinal arterioles may help shed light on the possible mechanisms contributing to the metabolic regulation of retinal blood flow under physiological and pathophysiological conditions.

3',5'-Cyclic-GMP Phosphodiesterases↗

PubMed1998

Lactate metabolism of subcutaneous adipose tissue studied by open flow microperfusion.

Open flow microperfusion and a novel calibration technique (ionic reference technique) were evaluated for the frequent measurement of the absolute lactate concentration in sc adipose tissue. Furthermore, the influence of the plasma insulin concentration on the lactate concentration of sc adipose tissue was investigated during hyperglycemia. Sixteen lean healthy young men participated in the studies. In the postabsorbtive state the mean sc lactate concentrations were 1.29 and 1.36 mmol/L for the ionic reference technique and the no net flux protocol, respectively (not significant, P > 0.05). The simultaneously measured arterialized plasma lactate concentration was significantly lower at 0.77 mmol/L (P < 0.05). Both the sc lactate concentration (1.8+/-0.33 mmol/L) and the plasma lactate concentration (0.96+/-0.03 mmol/L) were significantly elevated during a hyperinsulinemic euglycemic clamp experiment. During a hyperglycemic clamp experiment the sc lactate concentration reached a significantly elevated plateau (2.15+/-0.27 mmol/L) that was not influenced by the increasing plasma insulin concentration. It is concluded that 1) open flow microperfusion combined with the ionic reference technique enables frequent measurement of the sc lactate concentration; 2) sc adipose tissue is a significant source of lactate release in the postabsorbtive state as well as during hyperinsulinemic clamp conditions; and 3) insulin concentrations greater than 180 pmol/L have no further influence on adipocyte stimulation of sc adipose tissue with respect to lactate release.

Adipose Tissue↗

PubMed1996

1H- and 31P-nuclear magnetic resonance studies of l-lactate transport in isolated muscle fibers from the spiny lobster Panulirus argus

Proton (1H) and phosphorus (31P) nuclear magnetic resonance (NMR) spectroscopy were used to investigate the mode of transport of l-lactate across the plasma membranes of the abdominal extensor muscles of the spiny lobster Panulirus argus. Individual fibers or bundles of 23 fibers were superfused in a dual-tuned (1H, 31P) microsolenoid NMR probe. 1H-NMR spectra were diffusion-weighted, which eliminated the signal contribution of the fast-flowing extracellular lactate but retained that of intracellular lactate. Well-resolved intracellular lactate signals could be acquired at 15 s intervals, permitting estimation of initial velocities (Vi) of influx and efflux during loading/unloading of muscle fibers. 31P-NMR spectra were acquired to assess cellular energy status and intracellular pH. Transport results showed that Vi values for influx and efflux were a linear function of total lactate concentration, displaying no saturation effects. The rate of lactate influx was enhanced by increasing the concentration of the free acid by altering the superfusate pH. Vi values for influx and efflux of d- and l-lactate were identical. Finally, traditional inhibitors of monocarboxylate and/or anion transport had no effect on influx/efflux of lactate from these cells. The above results strongly suggest that the primary mode of lactate transport is by passive diffusion. These cells appear to lack a monocarboxylate transporter, which may be related to the apparent absence of organ-specific compartmentation of lactate metabolism in crustaceans.

Journal Article↗

PubMed1997

Lactate accumulation in the shell of the turtle Chrysemys picta bellii during anoxia at 3°C and 10°C

Lactate concentrations were measured in the shell and plasma of the turtle Chrysemys picta bellii after 3 months of submergence anoxia at 3°C and during and after 9 days of submergence anoxia at 10°C. Liver and skeletal muscle lactate levels were also measured in control and anoxic animals at each temperature. At 3°C, mean shell lactate concentration (N=4) reached 133mmolkg-1shellmass and plasma lactate levels were 144mmoll-1; at 10°C, shell and plasma lactate concentrations (N=5) rose in parallel during anoxic exposure, to 70.8mmolkg-1shellmass and 78.9mmoll-1, respectively, and returned in parallel to control levels during 9 days of recovery. At the end of the anoxic periods, an estimated 44% of the total body lactate resided in the shell at 3°C and 43% at 10°C, and indirect evidence suggests that the shell buffered these same fractions of the acid load. Because of the high lactate concentration per kilogram of shell water (416mmolkg-1 at 3°C; 221mmolkg-1 at 10°C) and the known formation of calcium lactate complexes, it is postulated that most of the lactate existed in the shell in combined form. I conclude that sequestration of lactate within the shell represents a potentially major adaptation to anoxic acidosis for this animal and, together with the previously described release of shell carbonates, may account for up to two-thirds of the total lactic acid buffering in this animal.

Journal Article↗

PubMed2003

The concept of maximal lactate steady state: a bridge between biochemistry, physiology and sport science.

The maximal lactate steady state (MLSS) is defined as the highest blood lactate concentration (MLSSc) and work load (MLSSw) that can be maintained over time without a continual blood lactate accumulation. A close relationship between endurance sport performance and MLSSw has been reported and the average velocity over a marathon is just below MLSSw. This work rate delineates the low- to high-intensity exercises at which carbohydrates contribute more than 50% of the total energy need and at which the fuel mix switches (crosses over) from predominantly fat to predominantly carbohydrate. The rate of metabolic adenosine triphosphate (ATP) turnover increases as a direct function of metabolic power output and the blood lactate at MLSS represents the highest point in the equilibrium between lactate appearance and disappearance both being equal to the lactate turnover. However, MLSSc has been reported to demonstrate a great variability between individuals (from 2-8 mmol/L) in capillary blood and not to be related to MLSSw. The fate of enhanced lactate clearance in trained individuals has been attributed primarily to oxidation in active muscle and gluconeogenesis in liver. The transport of lactate into and out of the cells is facilitated by monocarboxylate transporters (MCTs) which are transmembrane proteins and which are significantly improved by training. Endurance training increases the expression of MCT1 with intervariable effects on MCT4. The relationship between the concentration of the two MCTs and the performance parameters (i.e. the maximal distance run in 20 minutes) in elite athletes has not yet been reported. However, lactate exchange and removal indirectly estimated with velocity constants of the individual blood lactate recovery has been reported to be related to time to exhaustion at maximal oxygen uptake.

Adaptation, Physiological↗

PubMed2004

Lactate in solid malignant tumors: potential basis of a metabolic classification in clinical oncology.

A number of studies have demonstrated that malignant transformation is associated with an increase in glycolytic flux and in anaerobic and aerobic cellular lactate excretion. Using quantitative bioluminescence imaging in various primary carcinomas in patients (uterine cervix, head and neck, colorectal region) at first diagnosis of the disease, we showed that lactate concentrations in tumors in vivo could be relatively low or extremely high (up to 40 micromol/g) in different individual tumors or within the same lesion. In all tumor entities investigated, high molar concentrations of lactate were correlated with a high incidence of distant metastasis already in an early stage of the disease. Low lactate tumors (< median of approx. 8 micromol/g) were associated with both a longer overall and disease free survival compared to high lactate lesions (lactate > approx. 8 micromol/g). Lactate dehydrogenase was found to be upregulated in most of these tumors compared to surrounding normal tissue. Numerous recent reports support these data by demonstrating various biological activities of lactate that can enhance the malignant behavior of cancer cells. These mechanisms include the activation of hyaluronan synthesis by tumor-associated fibroblasts, upregulation of VEGF and of HIF-1 alpha, and direct enhancement of cellular motility which generates favorable conditions for metastatic spread. Thus, lactate accumulation not only mirrors but also actively enhances the degree of tumor malignancy. We propose that determination of lactate in primary tumors may serve as a basis for a novel metabolic classification which can lead to an improvement of prognosis and therapy in clinical oncology.

Animals↗

PubMed1997

Comparison of ethacridine lactate and prostaglandin E2 in second trimester medical abortion.

BACKGROUND: A comparison of ethacridine lactate and prostaglandin E2 (PGE2) with or without oxytocin infusion in second trimester medical abortion cases. METHODS: A prospective study was performed on 151 women requiring second trimester medical abortions between 1989 and 1995. Patients were randomly assigned to PGE2 group (n = 30), ethacridine lactate group (n = 48), ethacridine lactate combined with oxytocin infusion group (n = 49) and PGE2 combined with oxytocin infusion group (n = 24). Rates of successful abortion (i.e., complete evacuation of fetal and placental tissues from the uterus) within 24 hours for each group were determined and compared by chi2 and the Student t-test. RESULTS: Statistically significant difference concerning successful abortion rates was observed between ethacridine lactate and PGE2 groups, PGE2 and PGE2+oxytocin infusion groups, and ethacridine lactate+oxytocin infusion and PGE2 groups, while there was no significant difference between ethacridine lactate and ethacridine lactate+oxytocin infusion groups, ethacridine lactate and PGE2+oxytocin infusion groups, and PGE2+oxytocin infusion and ethacridine lactate+oxytocin infusion groups. CONCLUSIONS: Extra-amniotic ethacridine lactate instillation alone and intracervical PGE2 gel application are effective and safe methods for second trimester abortion.

Abortion, Induced↗

PubMed2005

Relationship between cerebral blood flow and oxygen metabolism, and extracellular glucose and lactate concentrations during middle cerebral artery occlusion and reperfusion: a microdialysis and positron emission tomography study in nonhuman primates.

OBJECT: Changes in lactate and glucose levels in the brain may be used to monitor a dynamic ischemic process. The authors related extracellular concentrations of glucose and lactate to regional cerebral blood flow (rCBF) and cerebral metabolic rate of oxygen (CMRO2) in a model of ischemia. METHODS: Transient (2 hours) middle cerebral artery occlusion (MCAO) was performed in eight macaque monkeys. Extracellular measurements of glucose and lactate levels using microdialysis (two probes in each brain) and sequential positron emission tomography measurements were performed during MCAO and reperfusion. Glucose and lactate levels were related to rCBF and CMRO2 as well as the pathophysiological categories of severe ischemia and penumbra. In probe regions characterized by severe ischemia, there were significant changes in glucose and lactate levels and the lactate/glucose ratio. In probe regions distinguished by penumbra, only lactate levels increased significantly and, in general, the changes were smaller and transient. This difference between severe ischemic and penumbral regions was significant for all microdialysis parameters. There was a significant correlation between glucose, and CBF and CMRO2. Lactate concentration was correlated with CMRO2. CONCLUSIONS: Extracellular glucose levels might be limited by rCBF, whereas lactate levels were more related to CMRO2. Lactate concentration is a better marker of irreversible ischemia than glucose concentration, although near-zero levels of glucose during MCAO probably signals near-complete cessation of rCBF. In situations with elevated lactate levels, glucose may help to discriminate between partial and severe ischemia.

Animals↗

PubMedDate not supplied

Lactate as a diagnostic test for septic peritoneal effusions in dogs and cats.

Lactate concentration in peritoneal fluid was evaluated and compared to blood lactate concentration in dogs and cats with septic and nonseptic abdominal effusions. All dogs with septic effusions had a peritoneal fluid lactate concentration >2.5 mmol/L and a peritoneal fluid lactate concentration higher than blood lactate, resulting in a negative blood to fluid lactate difference. In dogs, the diagnostic accuracy of the peritoneal fluid lactate concentration and the blood to fluid lactate difference in differentiating septic peritoneal effusion was 95% and 90%, respectively. Peritoneal fluid lactate concentration and blood to fluid lactate difference were not accurate tests for detecting septic peritoneal effusions in cats.

Animals↗

PubMed1998

[Relationship between plasma D(-)-lactate levels and acute intestinal injury in rats following ischemia-reperfusion].

OBJECTIVE: To determine the kinetics of plasma D(-)-lactate levels in both portal and systemic circulations, and to examine whether elevated plasma D(-)-lactate would correlate to intestinal injury in rats subjected to acute intestinal ischemia-reperfusion. METHODS: Anesthetized rats underwent 75 minutes of superior mesenteric artery occlusion followed by 6 hours of reperfusion. Plasma D(-)-lactate levels were measured by an enzymatic spectrophotometric assay. RESULTS: It showed that intestinal ischemia for 75 minutes resulted in a significant elevation in D(-)-lactate levels in portal vein blood compared to baseline values (P < 0.05). Plasma D(-)-lactate levels had a tendency to further increase after reperfusion up to 6 hours. Similar alterations in D(-)-lactate were also found in systemic circulation, there were no significant differences between the portal and systemic circulation at any time point. Moreover, the histopathological evaluation scores were significantly correlated to the portal D(-)-lactate levels in animals at various time points (r = 0.415, P < 0.01). In addition, a remarkable rise of endotoxin concentration within portal vein was already found at the end of 75-minute ischemia (P < 0.05), reaching a peak at 2 hours post-reperfusion. CONCLUSION: These data suggest that acute intestinal ischemia is associated with failure of mucosal barrier resulting in increased plasma D(-)-lactate levels in both portal and systemic blood. The subsequent reperfusion might cause further increase in D(-)-lactate levels, which correlated to the histopathological alterations. Plasma D(-)-lactate may be a useful marker of intestinal injury following both ischemia and reperfusion insults.

Animals↗