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PubMed1996

Changing effect of i.c.v. IL-1 beta on vasopressin release in anaesthetized, female rats at different stages of lactation: role of prostaglandins and noradrenaline.

Interleukin-1 beta stimulates oxytocin and vasopressin release in conscious, male rats and causes a rise in blood pressure. These experiments were done to : A) examine the effect of i.c.v. interleukin-1 beta (1 ng/microliter) on circulating levels of vasopressin in female rats at different stages of lactation and B) determine if alpha-adrenergic mechanisms and/or prostaglandins were involved as mediators. Urethane-anaesthetized nonlactating rats and rats at Day 7, 10, 20 and 26 of lactation were set up for arterial blood sampling and i.c.v. injections. One mL blood samples were obtained in one min periods before, and at 1, 2.5, 5, 10, 30, 60 and 120 min after the following treatments: i.c.v. treatment with either interleukin-1 beta (1 ng in 1 microliter PBS-BSA) or PBS-BSA (1 microliter) as a vehicle control; or i.c.v. treatment with interleukin-1 beta following pretreatment with either phentolamine (1.7 micrograms/microliter i.c.v.) or indomethacin (1 microgram/microliter i.c.v.). As blood was sampled, isotonic saline was infused (1 mL per min) and blood pressure was monitored to minimize any hypovolemic effects due to sampling. Extracted plasma was assayed using a specific vasopressin radioimmunoassay. Interleukin-1 beta i.c.v. stimulated the release of vasopressin above that elicited by PBS-BSA alone in non-lactating rats resulting in an approximate 1.2 to 2-fold increase in plasma hormone levels. Throughout the first half of lactation, vasopressin responsiveness to i.c.v. interleukin-1 beta treatment was markedly attenuated. In latter stages of lactation, the response recovered and resembled that of non-lactators around the time of weaning. Prostaglandins consistently mediate a stimulatory action of interleukin-1 beta on vasopressin release whereas alpha-adrenergic mechanisms mediate a depression of interleukin-1 beta-induced vasopressin release during the early to middle stages of lactation. It is possible that the depression in interleukin-1 beta-stimulation of vasopressin release in early to mid-lactation is conducive for nursing to occur and that the increase in vasopressin responsiveness towards the latter stages of lactation represents a component of the weaning process.

Anesthesia↗

PubMed1995

Lactate metabolism and hypocarbic hyperventilation. An experimental study in piglets.

Hyperventilation has been reported to increase blood lactate levels. Uncertainty exists as to whether high lactate levels are caused by increased peripheral release or decreased hepatic uptake. Seven piglets were investigated during controlled normoventilation and 13 piglets during controlled hyperventilation. Blood was drawn from catheters in the femoral artery and vein and in the hepatic vein. Blood flow was measured in the femoral artery by an electromagnetic flow meter and in the splanchnic area by indocyanine green extraction. In addition, repeated muscle biopsies from the hind limb and back muscles were taken. The mean PaCo2 was 5.4 in the normoventilated and 3.5 kPa in the hyperventilated group. The average hind limb oxygen uptake was the same in both groups. The arterial blood lactate concentration was significantly higher (P = 0.03) in the hyperventilated group (2.6 mmol.l-1) as compared to the normoventilated group (1.5 mmol.l-1). However, the release of lactate from the hind limb, and the muscular content of lactate were the same in both groups. Similar and unchanged skeletal muscle contents of glucose-6-phosphate, fructose-1,6-diphosphate, alpha-glycerophosphate, pyruvate, citrate and ATP were recorded in both groups. The splanchnic region did not take up or release lactate at normal PaCO2, but released lactate after 120 minutes of hyperventilation. The results indicate that the increased concentration of lactate during hypocarbic hyperventilation was not caused by an increased peripheral release from the skeletal muscles of the pig but could be caused by an altered splanchnic turn-over of lactate.

Adenosine Triphosphate↗

PubMed1991

Reduction in lactate accumulation correlates with differentiation-induced terminal cell division of leukemia cells.

Lactate accumulation in the medium and glucose utilization decreased during the induction of in vitro differentiation of mouse erythroleukemia (MEL) and human myeloid leukemia (HL-60) cells. The decrease in lactate accumulation occurred as early as 24 h after inducer treatment was initiated and occurred prior to the decrease in glucose utilization. The decrease in lactate accumulation was greater than that predicted by the decrease in glucose utilization, i.e., the ratio of glucose used glycolytically, as measured by lactate accumulation, to glucose used in other pathways ('glycolytic ratio') markedly decreased during differentiation in these cell lines. Differentiation correlated with the abrogation of the high levels of lactate accumulation first described by Warburg as characteristic of some transformed and neoplastic cells. Studies on both parental and differentiation-resistant variant MEL cell lines indicated that the changes in lactate accumulation were not dependent on the changes in glucose utilization and could be dissociated from them. Moreover, the changes in lactate accumulation only occurred in cells able to undergo differentiation-induced terminal cell division. This regulatable expression of lactate accumulation in MEL and HL-60 cells in vitro may make them useful model systems for the elucidation of the molecular mechanisms controlling lactate formation in malignant cells.

Acetamides↗

PubMed1979

Transport of D-lactate in perfused rat liver.

The transport of D-lactate across the plasma membrane was investigated in hemoglobin-free perfused rat livers, applying the multiple-indicator dilution technique (pulse labelling of D-lactate and indicator substances). The following results were obtained: 1. The steady state exchange rate at 1 mM D-lactate was 2.5 mumol x min-1 x g wet wt-1. It was proportional to the extracellular concentration in the range between 0.1 and 70 mM. 2. The transport of D-lactate was inhibited by L-lactate and pyruvate; 50% inhibition was observed at 40 mM L-lactate or 5 mM pyruvate. 3. The transport was also inhibited by alpha-cyanocinnamate and 4,4'-diisocyanostilbene-2,2'-disulfonic acid. The inhibition by cyanocinnamate was complete (with 25 mM) and fully reversible, whereas the inhibition by diisothiocyanostilbenedisulfonic acid was incomplete and irreversible; it was dependent upon the amount of diisothiocyanostilbenedisulfonic acid bound by the liver. Maximal inhibition (80%) was observed with 2 mumol diisothiocyanostilbenedisulfonic acid bound per g wet weight. 4. The intracellular concentration (ci) of D-lactate was proportional to the extracellular concentration (ce); the ratio ci/ce was 0.5 throughout the concentration range studied. It decreased in the presence of L-lactate or pyruvate. It is concluded that the transport of D-lactate is carrier-mediated, and, at least partially, electroneutral.

4-Acetamido-4'-isothiocyanatostilbene-2,2'-disulfo↗

PubMed1979

Metabolism of isolated kidney tubules. Interactions between lactate, glutamine and oleate metabolism.

Kidney-cortex tubule suspensions were prepared by collagenase treatment of kidney cortex from fed and starved rats. This preparation, consisting mainly of proximal convoluted tubules was incubated with three major renal substrates, L-lactate, glutamine and oleate to study the dose dependence of substrate uptake rates from medium substrate combinations. All three substances, when added at near physiological concentrations, modified the uptake rate and fate of the other substrates. In accordance with previous observations, oleate inhibited lactate uptake, and lactate decreased glutamine metabolism. Glutamine on the other hand led to a marked increase in lactate uptake. Both, glutamine and lactate increased oleate metabolism. Glucose was the main product of lactate and glutamine metabolism, lactate being preferentially taken up for this process. Oleate led to a net synthesis of triglycerides in the tubules, which was stimulated by the addition of lactate and glutamine. More than 75% of the oleate taken up was recovered as triglycerides. In the absence of fatty acids, triglyceride content of tubules decreased. The results indicate that oleate is taken up in preference to lactate and glutamine when all three substrates are offered to the tubule. Glucose and triglycerides are the main metabolic products of tubular substrate metabolism. Whereas glucose is released into the medium, triglycerides are stored in the tubule cell.

Animals↗

PubMed1982

Reduction of respiratory-chain cytochrome b by lactate in Saccharomyces cerevisiae.

Cytochrome b of yeast mitochondria can be reduced by a part of the electrons resulting from the oxidation of lactate enantiomers. 1. The respiration of D-lactate and L-lactate is 30-40% inhibited by antimycin A. 2. Reduction of cytochrome b is observed in submitochondrial particles in the presence of low concentration of D-lactate and L-lactate (half-optimal concentration of 4.7 mM and 2.4 mM respectively) in the presence of different bc1 inhibitors. 3. Reduction of cytochrome b and c1 occurs in purified complex III of yeast in the presence of L-lactate and added L-lactate: NAD+ oxidoreductase. 4. In the particles obtained from yeast grown in lactate the oxidation of L-lactate involves the reduction of a pigment absorbing at 558 nm.

Chemical Phenomena↗

PubMed1991

Protection of ischaemic synaptosomes from calcium overload by addition of exogenous lactate.

In depolarised anoxic synaptosomes, in which lactate production was significantly raised compared with normoxic conditions, calcium uptake, net acetylcholine release, and the intrasynaptosomal calcium concentration were all significantly lowered. In contrast, lactate production in synaptosomes incubated under aglycaemic- and ischaemic-type conditions was significantly lower and basal calcium uptake, acetylcholine release, and intrasynaptosomal calcium concentration were elevated compared with normoxia. In addition, the increase in intrasynaptosomal calcium concentration under the ischaemic-type condition appeared to be greater than could be accounted for by the rise in calcium uptake alone. Intrasynaptosomal pH reflected the lactate production under each condition investigated. Addition of exogenous lactate to normoxic synaptosomes mimicked the effects observed in anoxia, suggesting that lactate itself may have blocked the calcium uptake, inhibiting the rise in intrasynaptosomal calcium and acetylcholine release occurring in depolarised anoxic synaptosomes. When lactate was added to ischaemic synaptosomes, the large rise in intrasynaptosomal calcium concentration, calcium uptake, and acetylcholine release were decreased, suggesting that lactate may have a protective role in preventing cell death by calcium overload under ischaemic-type conditions. Evidence is presented to suggest that the effect of L-lactate was due to the lactate moiety itself rather than the associated acidosis.

Acetylcholine↗

PubMed1992

Extracellular intermediates of glucose metabolism: fluxes of endogenous lactate and alanine through extracellular pools in embryonic sympathetic ganglia.

The flux rates of lactate and alanine in and out of the cells of an intact tissue, which cannot be measured directly because some of the released materials are reabsorbed, were determined by computer analysis of uptakes and outputs by the whole tissue in the presence of various concentrations of these substances. The outputs of labeled lactate and alanine from [U-14C]glucose and the uptakes of [U-14C]lactate and [U-14C]alanine were measured on intact sympathetic ganglia excised from 15-day-old chicken embryos. The volume and time constant of the extracellular space were measured using labeled lactate, alanine, and sucrose. Models, which mathematically described the cellular uptakes and outputs as functions of the extracellular concentrations, were used to predict the exchanges that would be observed on the whole tissue, and their parameters were adjusted for best fit to the actual observations. The fitted models were then used to calculate the fluxes in and out of the cells and the concentrations in the extracellular space. The following results were obtained: (1) Cellular uptakes of lactate and alanine were both well described by familiar Michaelis-Menten kinetics. (2) The cellular output of [14C]-lactate from [14C]glucose declined with increase in the extracellular lactate concentration, whereas the cellular output of [14C]alanine from [14C]glucose rose with the extracellular alanine concentration. (3) Half-saturation values for cellular uptake, determined from the fitted equations, were 0.45 mM for lactate and 1.17 mM for alanine, both several-fold lower than less relevant estimates for the whole tissue made directly from the uptake observations. (4) As much as 45% of the carbon in the glucose consumed was released into the extracellular space as lactate and alanine, but much of this was reabsorbed. Implications for brain metabolism are discussed.

Alanine↗

PubMed1982

Pathophysiology of metabolic acidosis: effect of low pH on the hepatic uptake of lactate, pyruvate and alanine.

The uptake of lactate, pyruvate and alanine in perfused rat liver was investigated under normal perfusion conditions (pH 7.4, PCO2 40 mmHg) and under conditions mimicking partially compensated metabolic acidosis (pH 6.9, PCO2 20 mmHg). At 1 mM lactate as well as 10 mM lactate in the medium a lowering of pH from 7.4 to 6.9 did not affect the lactate plus pyruvate uptake. A significant effect of the low pH was seen on pyruvate uptake which at 1 mM lactate was increased from 0.027 +/- 0.008(4) mumol/min per g liver at normal pH to 0.084 +/- 0.013(4) at low pH. At 10 mM lactate the liver produced pyruvate, but the production was significantly reduced by a lowering of the pH, being 0.45 +/- 0.13(8) mumol/min per g liver at pH 7.4 and 0.22 +/- 0.06(4) at pH 6.9. THe counterbalancing changes in lactate metabolism were too small to attain statistical significance. The stimulation of gluconeogenesis by an increase in FFA from 0 to 1 mM in the medium was unaffected by pH. Alanine uptake was decreased from 0.48 +/- 0.05(6) to 0.39 +/- 0.07(3) by lowering the pH from 7.4 to 6.9. We conclude that metabolic acidosis does not in itself inhibit the capacity of the perfused rat liver to remove lactate and pyruvate from the blood. If the same is true in man, no beneficial effect of bicarbonate treatment on lactate clearance in patients with lactic acidosis should be expected.

Acidosis↗

PubMed1991

Muscle lactate transport studied in sarcolemmal giant vesicles: dependence on fibre type and age.

Lactate transport was studied in sarcolemmal giant vesicles obtained from rat or rabbit skeletal muscle. With this technique it is possible to obtain quantitative information on sarcolemmal transport characteristics. In equilibrium exchange experiments with 10, 30 and 60 mM lactate, vesicles from 'red' rat muscles had a 50% higher lactate transport capacity than vesicles from 'white' muscles. Giant vesicles made from rabbit red muscles had a 39% higher lactate transport capacity than vesicles from white muscles. These differences probably reflect a different number of lactate transporters, whereas the lactate affinity in red and white muscles are identical. Lactate transport capacity decreased with age. Sarcolemmal giant vesicles made from 22-month-old rats had a 28% lower transport capacity than vesicles from 2-month old rats. In absolute terms, the initial exchange flux with 30 mM lactate was 92 and 127 pmol cm-2 sec-1 for old and young rats, respectively. In supplementary studies in which microelectrode measurements were made in single mouse muscle fibers, it was shown that the cellular acidification rate due to lactate incubation, was 38% lower in fibres from 18-month old mice than in fibres from 2-month old mice.

Aging↗

PubMed1993

Potentiation of serotonin-induced contractility of gastric fundus strips in lactating rats.

Gastric fundus strips isolated from lactating, non-lactating and pregnant rats were used to obtain agonist-induced contractions in vitro and the mechanism of alteration in gastric contractility to serotonin during lactation was investigated. The gastric contractile responses to 5-HT expressed as area per unit mass of muscle (cm2 g-1 muscle) were 60-65% greater in lactating rats compared with non-lactating rats. However, responses evoked by acetylcholine (ACh) or histamine were not different. The EC50 values for 5-HT were not different in either group indicating that there was no alteration in the 5-HT affinity for its receptors in lactating rats. In pregnant rats, 5-HT-induced gastric responses were significantly (P < 0.05) lower than those of non-lactating rats. Pretreatment of non-lactating rats with haloperidol (which increases plasma prolactin levels) enhanced the gastric contractile response to 5-HT (P < 0.05). On the other hand bromocriptine administration (which lowers plasma prolactin levels) in lactating or immature rats, decreased the contractile response to 5-HT significantly, while bath application of bromocriptine (0.1 microM) had no effect. Incubation of fundus strips in physiological solution containing prolactin (10 micrograms ml-1) for 24 h decreased the 5-HT evoked contractions, but not the ACh evoked responses. The results in this study indicate that prolactin modulates the intrinsic contractile activity of the gastric smooth muscles to 5-HT.

Acetylcholine↗

PubMed1979

Lactation in the rabbit: mammary blood flow and cardiac output.

In anaesthetized rabbits, cardiac output (C.O.) and its distribution to the mammary glands, heart, liver and kidneys have been determined in established lactation (11--13 days), later lactation (26--27 days) and in virgins. During lactation, the volume of circulating blood, C.O., mammary blood flow and mammary weight were significantly greater than in virgins. There were no significant differences in C.O. and % C.O. received by the mammary glands between established and late lactation, and no significant decrease in mammary blood flow in late lactation. The weights of the liver and kidneys were significantly increased in lactation but there were no significant differences in liver, heart (coronary) and kidney blood flow. The rate of growth of the young was positively and significantly correlated with % C.O. received by the mammary glands and mammary weight, but not with C.O. Strong correlation was also observed between the % C.O. received by the mammary glands and mammary weight. There were no significant differences in C.O., mammary % C.O. and mammary blood flow in animals in established lactation 2--3 h and 24 h after suckling (i.e. shortly after and just before suckling). By 48 h after the last suckling mammary blood flow and % C.O., but not C.O., were significantly decreased. Possible factors causing these changes are discussed. The results are discussed in relation to the change in milk composition that occurs in late lactation in this species and to the role and effects of prolactin. It is suggested that events occurring during lactation have different sensitivities to prolactin.

Animals↗

PubMed1993

Changes in myoplasmic pH and calcium concentration during exposure to lactate in isolated rat ventricular myocytes.

1. We investigated the mechanisms involved in the rise of myoplasmic calcium concentration ([Ca2+]i) when isolated rat ventricular myocytes were exposed to lactate. The intracellular pH (pHi) and [Ca2+]i were measured using the fluorescent indicators 2',7'-bis(carboxyethyl)-5(6)-carboxyfluorescein (BCECF) and fura-2, respectively. Cell shortening was used as a measure of contractile performance. 2. Exposure to 20 mM lactate at the normal extracellular pH (pHo 7.4) for 10 min caused the pHi to fall rapidly by 0.24 pH units and cell shortening was reduced. Thereafter, pHi partially recovered by 0.16 pH units, which was paralleled by a recovery of shortening. 3. Exposure to lactate at a reduced extracellular pH (pHo 6.4) induced a very large acidosis of 0.70 pH units and cell shortening was abolished. During maintained exposure to lactate the pHi remained constant and cell shortening did not recover. 4. Application of Na(+)-H+ exchanger inhibitors, amiloride or ethylisopropyl-amiloride (EIPA), abolished the recovery of pHi and shortening during maintained exposure to lactate at pHo 7.4 and caused an additional acidosis during maintained application of lactate at pHo 6.4. 5. Application of lactate at both the normal and reduced pHo resulted in a rapid, followed by a slower, rise in [Ca2+]i. The diastolic and systolic [Ca2+]i and the amplitude of the systolic rise in the [Ca2+]i (the Ca2+ transient) all increased in both the rapid and the slow phase. 6. When lactate was applied at pHo 7.4, in the presence of EIPA, the initial rise of [Ca2+]i still occurred but the slower increase was abolished. This suggests an involvement of the Na(+)-H+ exchanger in the slower rise of [Ca2+]i. 7. In conclusion, the Na(+)-H+ exchanger is an important regulator of pHi during a lactate-induced intracellular acidosis. The rise of [Ca2+]i involves at least two mechanisms: (i) a rapid component which may represent reduced myoplasmic Ca2+ buffering, impaired Ca2+ removal by the sarcoplasmic reticulum or a direct inhibitory effect of protons on the Na(+)-Ca2+ exchanger; (ii) a slower component linked to stimulation of Na(+)-H+ exchanger which causes an increased [Na+]i and stimulates the Na(+)-Ca2+ exchanger, resulting in an enhanced Ca2+ influx.

Animals↗

PubMed1995

Analysis of bursting responses of oxytocin neurones in the rat in late pregnancy, lactation and after weaning.

1. Electrophysiological recordings were undertaken to compare bursting characteristics of oxytocin (OT) neurones at four reproductive stages: day 20 pregnancy, day 22 of pregnancy (expected day of parturition), day 7-11 of lactation, and day 5-6 after weaning. 2. Each OT neurone was recorded for 1 h of suckling, combined with cervico-vaginal probing at 5 min intervals as an additional stimulus for bursting. Intracerebroventricular (I.C.V.) oxytocin (2.2 ng) was given after 30 min to facilitate bursting responses. Bursts observed during suckling were classified as 'spontaneous' or 'probe-evoked'. 3. The percentage of cells displaying spontaneous and/or probe-evoked bursts during the recording was low in day 20 pregnant animals, high in lactators and intermediate in day 20 pregnant and weaner groups. These differences may relate to variation in the proportion of animals with a responsive milk-ejection reflex, as well as the relative size of the population of bursting OT neurones. 4. In the period before I.C.V. OT, overall burst frequency (including both spontaneous and probe-evoked bursts) was similar across groups. After I.C.V. OT, overall burst frequency was much higher in lactators compared with other groups. Similar results were obtained when spontaneous bursts were analysed separately. 5. Burst amplitude (action potentials per burst, including both spontaneous and probe-evoked bursts) prior to I.C.V. OT was similar between the day 20 pregnant, day 22 pregnant and lactating groups, but was lower in weaners. All groups showed an increase in burst amplitude after I.C.V. OT, but values in weaners remained lower than in other groups. In a separate analysis of spontaneous bursts, burst amplitude after I.C.V. OT was higher in lactators, and lower in weaners, than in pregnant animals. 6. Background firing rates of OT cells were higher in the day 20 and day 22 pregnant groups compared with lactators, and lower in weaners. Only OT cells in lactators showed a significant increase in background firing rates following I.C.V. OT. 7. It is concluded that the bursting characteristics of OT cells change markedly between late pregnancy, mid-lactation and weaning. The factors underlying these changes, which are only loosely correlated with the sequence of morphological adaptations in OT cells surrounding lactation, remain to be established.

Action Potentials↗

PubMed2002

No evidence of an intracellular lactate shuttle in rat skeletal muscle.

The concerted view is that cytosolic pyruvate is transferred into mitochondria and after oxidative decarboxylation further metabolized in the tricarboxylic acid cycle. Recently this view has been challenged. Based on experimental evidence from rat skeletal muscle it has been concluded that mitochondria predominantly oxidize lactate in vivo and that this constitutes part of an 'intracellular lactate shuttle'. This view appears to be gaining acceptance in the scientific community and due to its conceptual importance, confirmation by independent experiments is required. We have repeated the experiments in mitochondria isolated from rat soleus muscle. Contrary to the previously published findings we cannot find any mitochondrial respiration with lactate. Analysis of lactate dehydrogenase (LDH) by spectrophotometry demonstrated that the activity in the mitochondrial fraction was only 0.7 % of total activity. However, even when external LDH was added to mitochondria, there were no signs of respiration with lactate. In the presence of conditions where lactate is converted to pyruvate (external additions of both LDH and NAD(+)), mitochondrial oxygen consumption increased. Furthermore, we provide theoretical evidence that direct mitochondrial lactate oxidation is energetically unlikely. Based on the present data we conclude that direct mitochondrial lactate oxidation does not occur in skeletal muscle. The presence of an 'intracellular lactate shuttle' can therefore be questioned.

Animals↗

PubMed1969

Multiple forms of lactate dehydrogenase in Staphylococcus aureus.

Activities for nicotinamide adenine dinucleotide (NAD)-dependent and NAD-independent forms of lactate dehydrogenase (LDH) were measured in cell-free extracts of Staphylococcus aureus strain PS 6 for the d and l isomers of lactate. Data obtained for the NAD-dependent lactate dehydrogenases indicate that oxidation of both isomers of lactate is due to both an l-lactate-specific LDH and a lactate racemase. After acrylamide gel electrophoresis, two bands exhibiting LDH activity were detected in crude or in partially purified cell-free extracts. The fast band exhibited LDH activity that was not NAD-dependent for both isomers of lactate, whereas, the slow band had very high NAD-dependent LDH activity for the l isomer but just detectable activity or the d isomer. Both bands appeared when d-lactate was used as the substrate, but only the slow band was formed when l-lactate was the substrate. NAD-dependent LDH, in apparent association with a nonspecific tetrazolium-reducing protein, is responsible for the production of the slow band.

Cell-Free System↗

PubMed1996

Use of the relationship between blood lactate and running speed to determine the exercise intensity of horses.

Eight thoroughbred horses, trained for racing competition, were subjected to a standardised incremental speed test to determine the relationship between their blood lactate concentrations and running speed. Between 14 days before and 14 days after completing the standardised exercise test, the horses were timed for runs of 2000 to 6000 m. The blood lactate concentration after each run was measured and compared with the blood lactate concentration predicted from the individual horse's blood lactate-running speed relationship curve determined from the standardised exercise test. The relationship between the predicted and measured lactate concentrations was evaluated by linear regression. For 42 exercise runs there was a significant positive correlation between the measured and the predicted lactate concentrations and a significant regression: measured lactate (mmol/litre) = 1.01 predicted lactate (mmol/litre) -0.36 (r2 = 0.79, standard error of estimate 0-63 mmol/litre, P < 0.001). It was concluded that the standardised exercise test was a useful technique for predicting the blood lactate concentrations of horses after field exercise.

Animals↗

PubMed1977

Glucose and lactate kinetics in burn shock.

We studied the glucose and lactate kinetics during burn shock by means of the primed constant infusion of [6-3H]glucose and Na-L-(+)-[U-14C]lactate. We found an early postburn hyperglycemia that was due to an increased rate of appearance (Ra) of glucose. Later, the ability of the tissues to extract glucose became impaired, and the plasma glucose concentration increased even more in spite of the return of Ra of glucose to the control level. The Ra of lactate rose rapidly postburn, whereas the rate of disappearance (Rd) of lactate stayed at the control level for 30 min. Consequently, plasma lactate rose approximately 350%. After 30 min, Rd of lactate increased to the same level as Ra; and Ra, Rd, plasma lactate concentration, and the percent of glucose derived from lactate remained elevated for the duration of the experiment. These results indicate an important role of lactate in burn shock metabolism and substrate kinetics.

Animals↗