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PubMed2002

Postexercise red cell aggregation is negatively correlated with blood lactate rate of disappearance.

In three separate studies, we have observed that the rise in blood lactate during exercise is correlated to blood viscosity and red cell aggregation. Whether these results were related to an effect of blood rheology on lactate production by muscles or on lactate disappearance remains unknown. The modelling of postexercise lactate kinetics allows a fair evaluation of lactate production by muscles (gamma1) and lactate disappearance (gamma2), the latter being easily measurable with simplified protocols. We thus investigated the relationships between pre- and postexercise blood rheology and gamma2. Ten subjects (2 female and 8 males; age 16-45 yr, weight 62-106.5 kg) exhibiting a wide range of gamma2 (from 2 to 7.7x10(-2) min(-1)) underwent a maximal exercise-test with postexercise calculation of gamma2 with the simplified formula gamma2=0.0724+0.755(Lac8-Lac20)/(Lac8.Deltat)-0.00684Lac20 where Lac8 and Lac20 are lactate concentrations 8 and 10 min after exercise stop at the level of VO2max, as previously reported. During exercise whole blood viscosity eta(b) increased (+15%, p<0.01) due to a rise in hematocrit (p<0.05) and plasma viscosity (+0.08+/-0.03 mPa.s, p<0.05), while red cell rigidity was unchanged. Red cell aggregation (Myrenne M1) increased by 11% (p<0.05). Postexercise M1 (measured at VO2max) was the only hemorheologic parameter correlated to gamma2 (r=-0.697, p=0.037). We find once again a statistical relationship between lactate at exercise and red cell aggregation. Microcirculatory adaptations influenced by red cell aggregation may influence lactate disposal (as reflected by gamma2), adding its effect to that of the balance between carbohydrates and fat oxidation which is the major determinant of blood lactate concentrations at exercise in physiological conditions.

Adult↗
PubMed2004

Effects of acute hypoxia on the estimation of lactate threshold from ventilatory gas exchange indices during an incremental exercise test.

The purpose of this study was to investigate the validity of non-invasive lactate threshold estimation using ventilatory and pulmonary gas exchange indices under condition of acute hypoxia. Seven untrained males (21.4+/-1.2 years) performed two incremental exercise tests using an electromagnetically braked cycle ergometer: one breathing room air and other breathing 12 % O2. The lactate threshold was estimated using the following parameters: increase of ventilatory equivalent for O2 (VE/VO2) without increase of ventilatory equivalent for CO2 (VE/VCO2). It was also determined from the increase in blood lactate and decrease in standard bicarbonate. The VE/VO2 and lactate increase methods yielded the respective values for lactate threshold: 1.91+/-0.10 l/min (for the VE/VO2) vs. 1.89+/-0.1 l/min (for the lactate). However, in hypoxic condition, VE/VO2 started to increase prior to the actual threshold as determined from blood lactate response: 1.67+/-0.1 l/min (for the lactate) vs. 1.37+/-0.09 l/min (for the VE/VO2) (P=0.0001), i.e. resulted in pseudo-threshold behavior. In conclusion, the ventilatory and gas exchange indices provide an accurate lactate threshold. Although the potential for pseudo-threshold behavior of the standard ventilatory and gas exchange indices of the lactate threshold must be concerned if an incremental test is performed under hypoxic conditions in which carotid body chemosensitivity is increased.

Acute Disease↗
PubMed2005

Effect of J coupling and T2 Relaxation in Assessing of Methyl Lactate Signal using PRESS Sequence MR Spectroscopy.

PURPOSE: This work was aimed at quantification of lactate concentration using proton MR spectroscopy (MRS). We carried out a basic study to clarify the characteristics of signal change and T2 relaxation time of lactate that occur by J coupling in point resolved spectroscopy (PRESS) sequence. MATERIALS AND METHODS: Proton MRS was done for a water phantom containing 10 mmol/L creatine and lactate on a clinical 1.5 T MR system by using an asymmetric PRESS sequence. The coupling constant J was 7.35 Hz. In acquisitions, TE was varied from 68 ms up to 544 ms, with an increment of 68 ms (1/2J) and TR was fixed to 10000 ms. RESULTS: The shape and signal intensity of the lactate signal vary depending on its phase. The lactate signal intensity at TE 272 ms was higher than at TE 136 ms despite the longer TE. T2 relaxation times of lactate in the negative in-phase (TE 136 ms, TE 408 ms) and positive in-phase (TE 272 ms, TE 544 ms) were 1033 ms and 1042 ms, respectively (no significant differences), so that when the same phase was used, regardless of the phase condition, T2 relaxation behavior was not different. We considered that our results included over expression and loss of lactate signal depending on the phase. CONCLUSIONS: For evaluation of the lactate peak, we recommend the use of the positive in-phase signal because it is larger than the negative in-phase signal. The influence of the asymmetric PRESS sequence, which may cause loss and over expression of lactate signal, should be considered in the calculation of the quantification. The T2 relaxation time should be also considered in the calculation of the lactate value since it affects the value considerably.

Humans↗
PubMed1975

Lactate dehydrogenases in cyanobacteria.

NAD-linked lactate dehydrogenases specific for the D- and L-lactate have been demonstrated in a number of strains of unicellular cyanobacteria. The D-lactate dehydrogenase of one strain (Synechococcus 6716) was partially purified and its properties were studied. The enzyme has a molecular weight of ca. 115000-120000, is highly specific, autooxidizable, and susceptible to inhibition by iodoacetamide, oxamate and ATP. The possible physiological functions of the enzyme in the metabolism of the organism were investigated. D-lactate carbon was incorporated in cell material during photosynthetic growth with CO2, but lactate was not used as sole source for carbon for photosynthetic or chemosynthetic development. D-lactate and pyruvate were oxidized aerobically in the dark by resting cell suspensions with the assimilation mainly of the C2 and the C3 carbon atoms. In the oxidation of lactate, acetate was excreted into the medium. No fermentation of glucose was found, but a small amount of D-lactate was detected as a product of endogenous dark metabolism of the cell. All enzymes required for the production of lactate from glucose and from glycogen were found in exponentially growing cells, but the activity of some key enzymes was low or undetectable in old cultures.

Acetates↗
PubMed2000

Brain function rescue effect of lactate following hypoglycaemia is not an adaptation process in both normal and type I diabetic subjects.

AIMS/HYPOTHESIS: We have previously shown that lactate protects brain function during insulin-induced hypoglycaemia. An adaptation process could, however, not be excluded because the blood lactate increase preceded hypoglycaemia. METHODS: We studied seven healthy volunteers and seven patients with Type I (insulin-dependent) diabetes mellitus with a hyperinsulinaemic (1.5 mU.kg-1.min-1) stepwise hypoglycaemic clamp (4.8 to 3.6, 3.0 and 2.8 mmol/l) with and without Na-lactate infusion (30 mumol.kg-1.min-1) given after initiation of hypoglycaemic symptoms. RESULTS: The glucose threshold for epinephrine response was similar (control subjects 3.2 +/- 0.1 vs 3.2 +/- 0.1, diabetic patients = 3.5 +/- 0.1 vs 3.5 +/- 0.1 mmol/l) in both studies. The magnitude of the response was, however, blunted by lactate infusion (AUC; control subjects 65 +/- 28 vs 314 +/- 55 nmol/l/180 min, zenith = 2.6 +/- 0.5 vs 4.8 +/- 0.7 nmol/l, p < 0.05; diabetic patients = 102 +/- 14 vs 205 +/- 40 nmol/l/180 min, zenith = 1.4 +/- 0.4 vs 3.2 +/- 0.3 nmol/l, p < 0.01). The glucose threshold for symptoms was also similar (C = autonomic 3.0 +/- 0.1 vs 3.0 +/- 0.1, neuroglycopenic = 2.8 +/- 0.1 vs 2.9 +/- 0.1 mmol/l, D = autonomic 3.2 +/- 0.1 vs 3.2 +/- 0.1, neuroglycopenic 3.1 +/- 0.1 vs 3.2 +/- 0.1 mmol/l) but peak responses were significantly attenuated by lactate (score at 160 min C = 2.6 +/- 1 vs 8.8 +/- 1, and 0.4 +/- 0.4 vs 4.8 +/- 1, respectively; p = 0.02-0.01, D = 1.3 +/- 0.5 vs 6.3 +/- 1.7, and 2.3 +/- 0.6 vs 5.7 +/- 1.1 p = 0.07-0.02). Cognitive function deteriorated in both studies at similar glucose thresholds (C = 3.1 +/- 0.1 vs 3.0 +/- 0.1, D = 3.2 +/- 0.1 vs 3.3 +/- 0.2 mmol/l). Although in normal subjects a much smaller impairment was observed with lactate infusion (delta four-choice reaction time at 160 min = 22 +/- 12 vs 77 +/- 31 ms; p = 0.02), in Type I diabetic patients lactate infusion was associated with an improvement in cognitive dysfunction (0.2 +/- 0.4 vs -38 +/- 0.2 delta ms, p = 0.0001). CONCLUSION/INTERPRETATION: A blood lactate increase after the development of hypoglycaemic symptoms reduces counterregulatory and symptomatic responses to insulin-induced hypoglycaemia and favours brain function rescue both in normal and diabetic subjects. These findings confirm that lactate is an alternative substrate to glucose for cerebral metabolism under hypoglycaemic conditions.

Acclimatization↗
PubMed1991

Kinetic mechanism of the endogenous lactate dehydrogenase activity of duck epsilon-crystallin.

Initial velocity, product inhibition, and substrate inhibition studies suggest that the endogenous lactate dehydrogenase activity of duck epsilon-crystallin follows an order Bi-Bi sequential mechanism. In the forward reaction (pyruvate reduction), substrate inhibition by pyruvate was uncompetitive with inhibition constant of 6.7 +/- 1.7 mM. In the reverse reaction (lactate oxidation), substrate inhibition by L-lactate was uncompetitive with inhibition constant of 158 +/- 25 mM. The cause of these inhibitions may be due to epsilon-crystallin-NAD(+)-pyruvate and epsilon-crystallin-NADH-L-lactate abortive ternary complex formation as suggested by the multiple inhibition studies. Pyruvate binds to free enzyme very poorly, with a very large dissociation constant. Bromopyruvate, fluoropyruvate, pyruvate methyl ester, and pyruvate ethyl ester are alternative substrates for pyruvate. 3-Acetylpyridine adenine dinucleotide, nicotinamide 1,N6-ethenoadenine dinucleotide, and nicotinamide hypoxanthine dinucleotide serve as alternative coenzymes for epsilon-crystallin. All the above alternative substrates or coenzymes showed an intersecting initial-velocity pattern conforming to the order Bi--Bi kinetic mechanism. Nicotinic acid adenine dinucleotide, thionicotinamide adenine dinucleotide, and 3-aminopyridine adenine dinucleotide acted as inhibitors for this enzymatic crystallin. The inhibitors were competitive versus NAD+ and noncompetitive versus L-lactate. alpha-NAD+ was a noncompetitive inhibitor with respect to the usual beta-NAD+. D-Lactate, tartronate, and oxamate were strong dead-end inhibitors for the lactate dehydrogenase activity of epsilon-crystallin. Both D-lactate and tartronate were competitive inhibitors versus L-lactate while oxamate was a competitive inhibitor versus pyruvate. We conclude that the structural requirements for the substrate and coenzyme of epsilon-crystallin are similar to those of other dehydrogenases and that the carboxamide carbonyl group of the nicotinamide moiety is important for the coenzyme activity.

Animals↗
PubMed1979

[Diagnostic significance of lactate concentration in CSF in patients with meningitis (author's transl)].

White-cell count and differential blood count, total protein, lactate dehydrogenase activity (E.C. 1.1.1.27) and lactate concentration were determined in 496 CSF samples, obtained by lumbar puncture. Lactate was measured with a new enzymatic test. Reference values were determined for lactate and lactate dehydrogenase (90% limits: 1.2-2.1 mmol/l and 6-26 U/l, respectively). Lactate content proved to be best in the differential diagnosis between acute bacterial and abacterial meningitis: concentrations of 3.5 mmol/ml and above were found exclusively in bacterial meningitis. As for other diseases, markedly increased lactate concentrations were measured only in patients with brain tumour or cerebrovascular disease (up to 9.3 mmol/l). Determination of lactate concentration alone would have led to a misdiagnosis of acute bacterial meningitis in 3% of cases. If the CSF contains 3.5 mmol/l lactate or more and the leucocyte cell count is above 800/microliter, brain tumour or cerebrovascular disease can be practically excluded and the diagnosis of bacterial meningitis made with a high degree of reliability.

Adolescent↗
PubMed1993

Lactated Ringer's solution alleviates brain trauma-precipitated lactic acidosis in hemorrhagic shock.

To determine the influence of brain trauma on blood acid-base and lactate-pyruvate responses to hemorrhage, and the effect of lactated Ringer's solution on these responses, 30 anesthetized rats were assigned to four groups: hemorrhage (n = 7), hemorrhage following fluid percussion brain trauma (trauma-hemorrhage group) (n = 7), hemorrhage treated with lactated Ringer's solution (hemorrhage-resuscitation group) (n = 8), and hemorrhage following brain trauma treated with lactated Ringer's solution (trauma-hemorrhage-resuscitation group) (n = 8). The hemorrhage group showed no significant changes in pH, HCO3, and base excess after hemorrhage. Base excess and pH were significantly reduced after the hemorrhage in the trauma-hemorrhage group but were raised after resuscitation in the hemorrhage-resuscitation group. Acid-base values showed no difference between the trauma-hemorrhage-resuscitation and hemorrhage groups. The trauma-hemorrhage-resuscitation group also had a significantly higher base excess than the trauma-hemorrhage group. Lactate rose significantly after hemorrhage in the hemorrhage group and was even higher in the trauma-hemorrhage group, but there were no differences between the hemorrhage versus hemorrhage-resuscitation or trauma-hemorrhage-resuscitation groups. Both brain trauma and lactated Ringer's solution increased pyruvate with marked reduction in the ratio of lactate to pyruvate. These data indicate that brain trauma precipitates blood lactate accumulation and metabolic acidosis after hemorrhage, and infusion of lactated Ringer's solution can relieve these disturbances.

Acidosis, Lactic↗
PubMed1993

The effects of exogenous lactate and pyruvate on the recovery of coronary flow in the rat heart after ischaemia.

OBJECTIVE: The effect of exogenous lactate and pyruvate on the recovery of coronary flow (total, regional) after ischaemia as a function of the duration of ischaemia was evaluated. METHODS: Isolated, ejecting rat hearts were subjected to ischaemia for 15, 30, or 45 minutes. Glucose (11 mM) was present as the basal substrate in the perfusion medium and lactate (5 mM) or pyruvate (5 mM) was added as the cosubstrate. Flow variables were measured by the timed collection of coronary effluents and by the radioactive microsphere technique. RESULTS: In the lactate perfused hearts, reactive hyperaemia was present after 15 minutes but absent after 30 and 45 minutes of ischaemia. Total coronary flow was significantly reduced after 45 minutes of ischaemia. Transmural flow was impaired after 15, 30, and 45 minutes of ischaemia in the lactate perfused hearts, -that is, flow in the inner layers of the left ventricle was transiently reduced after 15 minutes and remained continuously depressed after 30 and 45 minutes of ischaemia. The pyruvate perfused hearts showed reactive hyperaemia after 15 and 30 minutes of ischaemia. After 45 minutes total coronary flow was reduced below the value before ischaemia, and in particular, the inner layers of the left ventricle were severely deprived of flow as in lactate perfused hearts. When neither lactate nor pyruvate was added to the perfusion medium (containing glucose), impairment of coronary flow in the inner layers of the left ventricle was only transiently obvious after 30 and 45 minutes of ischaemia. Impaired perfusion of the inner layers during reperfusion resulted in delayed washout of lactate dehydrogenase. CONCLUSIONS: Exogenous substrates modify the recovery of flow after ischaemia. In the presence of exogenous lactate, severe disturbances of flow are already obvious after 30 minutes of ischaemia in the inner layers of the left ventricle. Exogenous pyruvate delays impairment of flow in the inner layers compared with exogenous lactate.

Animals↗
PubMed2002

Metabolic and hemodynamic effects of hypertonic solutions: sodium-lactate versus sodium chloride infusion in postoperative patients.

Although hypertonic saline has been proposed as an intravenous resuscitation fluid, the beneficial effects of the sodium load are associated with potentially deleterious effects of chloride. Since the physiological lactate anion is well metabolized, hypertonic lactate solution could represent an interesting alternative. The aim of this study was to compare metabolic and hemodynamic effects of hypertonic infusion of sodium lactate versus sodium chloride in three groups of surgical patients who underwent elective coronary artery bypass grafting (CABG). Hypertonic lactate solution was infused to patients 14 to 16 h after surgery either involving a cardiopulmonary bypass (CPB-Lac, n = 20) or on-off pump (OPCAB-Lac, n = 20), whereas the third group consisted of patients undergoing cardiopulmonary bypass but receiving hypertonic saline solution (CPB-NaCl, n = 20). An equal fluid and sodium load (2.5 mL/2.5 mmol x kg(-1)) was infused in all patients over 15 min. Plasma glucose and sodium increased after infusion in the three groups, but the changes, although significant, were small. As expected, lactate rose only in CPB-Lac and OPCAB-Lac groups, the changes being more marked in CPB-Lac, indicating a slower lactate metabolism in this group compared with OPCAB-Lac. Although both solutions produced significant increases in cardiac index and oxygen delivery, there was a significant decrease in oxygen extraction only in groups receiving sodium lactate (CPB-Lac and OPCAB-Lac) and not in CPB-NaCl. Finally, hypertonic NaCl infusion induced a modest, although significant, decrease in arterial pH and bicarbonate, whereas hypertonic lactate infusion increased these two parameters in both CPB-Lac and OPCAB-Lac. This study demonstrates that hypertonic lactate infusion is safe and well tolerated in patients undergoing elective cardiac surgery.

Acid-Base Equilibrium↗
PubMed1996

Catabolic pathway for aerobic degradation of lactate by Actinomyces naeslundii.

The aerobic metabolism of lactate by oral Actinomyces was studied. Six of 7 strains of Actinomyces naeslundii increased their growth in the presence of lactate under aerobic conditions. Washed cells grown on lactate aerobically degraded lactate and pyruvate to acetate with a concomitant consumption of oxygen. In the presence of catalase, the molar ratios of oxygen consumed to acetate produced were 1 for lactate degradation and 0.5 for pyruvate degradation. The enzymatic activities found in cell extracts revealed that lactate could be converted to pyruvate by NAD-independent lactate dehydrogenase (iLDH) and further to acetyl CoA by pyruvate dehydrogenase (PDH). The acetyl CoA formed could be metabolized into acetate by phosphotransacetylase (PTA) and acetate kinase (AK) with the formation of ATP. These results indicate that A. naeslundii metabolizes lactate into acetate by the sequential enzymatic reactions iLDH, PDH, PTA and AK and that hydrogens produced by iLDH and PDH are transferred to oxygen. The activity of lactate degradation and oxygen consumption may modify the environmental conditions of dental plaque.

Acetate Kinase↗
PubMed1971

Influence of carboxylic acids on the stereospecific nicotinamide adenine dinucleotide-dependent and nicotinamide adenine dinucleotide-independent lactate dehydrogenases of Leuconostoc mesenteroides.

Leuconostoc mesenteroides increased its lactic acid production from glucose threefold when malic acid was added to the culture. This increase resulted also in a reduction of the ratio of d-lactic acid to l-lactic acid (31.5 to 1.23). Addition of malic acid increased 6.5-fold the specific activity of nicotinamide adenine dinucleotide (NAD)-linked l-lactate dehydrogenase and increased 3.2-fold that of NAD-linked d-lactate dehydrogenase. The Michaelis constant (K(m)) for NAD of the NAD-linked l-lactate dehydrogenase increased with the addition of malate, but no change was observed in the K(m) values for the respective d-enzyme. The effect of carboxylic acids on the NAD-linked l-lactate dehydrogenase activities was tested by using partially purified enzyme preparations from cells grown with glucose alone and from cells grown with glucose plus malate. Malate stimulated the l-enzyme and inhibited the d-lactate dehydrogenase. The NAD-linked l-lactate dehydrogenase exhibited the same activity bands on polyacrylamide gel electrophoresis whether the cell-free preparation originated from cells grown on glucose plus malate or on glucose as the sole carbon source. The NAD-linked d-lactate dehydrogenase, however, exhibited a different pattern of electrophoretic mobility, depending upon the source of origin of the cell-free preparation. The results suggest that malate has a stimulatory effect on the synthesis of both enzymes and may result in rearrangement of the protein structure of the d-lactate dehydrogenase. This rearrangement apparently makes the d-enzyme more susceptible to inhibition of catalytic activity. The l-lactate dehydrogenase, however, is stimulated not only in its synthesis but also in its activity. It is proposed that these effects are responsible for the regulation of lactic acid production.

Acids↗
PubMed1976

Effect of reaction initiator on human lactate dehydrogenase assay.

Human lactate dehydrogenase isoenzymes I and V have decreased activities when the reaction is initiated with lactate. No loss in lactate dehydrogenase I activity was found when the reaction was initiated with enzyme or NAD+. For lactate dehydrogenase V an NAD+-initiated reaction, as compared to an enzyme-initiated reaction, yields lower activity in sodium pyrophosphate buffer but higher activity in tris(hydroxymethyl)aminomethane buffer. Both isoenzymes have higher lactate-to-pyruvate activity when assayed in the latter buffer than when assayed in the former. Human lactate dehydrogenase V (but not I) exhibited different activities when assayed with lactate from two different commercial sources. Human lactate dehydrogenase assayed by the pyruvate-to-lactate reaction is not affected by the choice of reaction initiator.

Humans↗
PubMed1999

Daily energy expenditure across the course of lactation among urban Bangladeshi women.

Measures of energy intake of lactating women in developing countries show that intakes are often lower than those recommended by international bodies, while fat-mass losses are often substantially less than the 3-4 kg used in the calculations of recommendations, suggesting that physiological adaptation must be commonplace among such women. The cost of lactation may be met by reduction in energy expenditure, including reduced physical activity, as well as by mobilization of bodily soft tissue. However, daily energy expenditure of lactating women has been shown to increase across the course of lactation among women in a rural population in the Philippines and an urban population in India, with a decline in body weight across the course of lactation in both studies. In the present study, total daily energy expenditure and anthropometric body composition were measured longitudinally in 68 mothers from a poor urban area of Dhaka, Bangladesh, at 0, 1, 2, 4, and 8 months of lactation, to determine whether the increasing energy expenditure across lactation observed elsewhere also occurs in Bangladeshi women. In addition, the extent to which an extended period of lactation was accompanied by weight and body fat change in these women was determined. Energy expenditure by heart-rate monitoring and activity report, and body composition from anthropometry was carried out four times across the 8-month period of lactation. A small decline in body fat mass and a significant increase in total energy expenditure across this period were observed, confirming similar observations elsewhere in the developing world.

Adult↗
PubMed1982

The role of altered lactate kinetics in the pathogenesis of type B lactic acidosis.

Of the two types of lactic acidosis, Type B is the most difficult to explain in terms of mechanisms of lactic acid accumulation because the tissue hypoxia that accompanies Type A is not present except as a terminal event. The methods of pharmacokinetics show that for lactate to accumulate to an extent that would disturb acid-base balance, either lactate synthesis or lactate removal would have to be increased or decreased, respectively, by about 7-10-fold. To produce lactic acidosis within a few hours, synthesis would have to increase at the same time as clearance decreased. At normal contribution of the liver to the total lactate clearance (30%-40%), a total cessation of hepatic lactate clearance would not result in lactic acidosis without a concomitant rise in the rate of lactate synthesis. Again, to produce an acidosis this increase would have to be about 8-fold at a normal fractional hepatic clearance. The control of hepatic lactate uptake is discussed in the light of the relatively low hepatic extraction of lactate and in relation to to two main models of hepatic drug (lactate) clearance; the 'well-stirred' and 'parallel-tube' models.

Acidosis↗
PubMed1997

1H-magnetic resonance spectroscopy-determined cerebral lactate and poor neurological outcomes in children with central nervous system disease.

By using proton magnetic resonance spectroscopy ((1)H-MRS), cerebral lactate has been shown to be elevated in a wide variety of pediatric and adult neurological diseases. In this study we compared 36 newborns, infants, and children with elevated lactate peaks on (1)H-MRS with 61 patients without an identifiable lactate signal. (1)H-MRS was acquired from the occipital gray and parietal white matter (8 cm3 volume, STEAM sequence with echo time = 20 msec, repetition time = 3.0 seconds) and data were expressed as ratios of different metabolite peak areas (N-acetylaspartate [NA]/creatine [Cr], NA/choline [Ch], and Ch/Cr) and the presence of a characteristic lactate doublet peak at 1.3 ppm. Outcomes (Pediatric Cerebral Performance Category Scale score; PCPCS) were assigned 6 to 12 months after injury. Patients with lactate peaks were more likely to have suffered a cardiac arrest, were more often hyperglycemic, and had lower Glasgow Coma Scale scores on admission. They were also more likely to have abnormal metabolite ratios when compared with age-matched controls or with patients without detectable lactate. Of prognostic importance, patients with increased lactate were more likely to be severely disabled (39% vs 10%), survive in a persistent vegetative state (13% vs 2%), or have died (39% vs 7%). In contrast, patients with similar conditions without increased lactate were more likely to have had a good outcome (23% vs 3%) or recovered to a mild (38% vs 6%) or moderate disability (20% vs 0%). Our data suggest that (1)H-MRS is useful in the prediction of long-term outcomes in children with neurological disorders. Patients with elevated cerebral lactate are more likely to die acutely or are at greater risk for serious long-term disability.

Brain Diseases↗
PubMed1982

Metabolism of immunoglobulin A in lactating mice: origins of immunoglobulin A in milk.

The metabolism of albumin and IgA was studied in normal and lactationg mice. Lactation resulted in significant changes in the metabolism of these proteins. The serum albumin concentration was lowered from 47 mg/ml in normals to 24 mg/ml in lactating mice. However, only a slight decrease in the serum concentration of IgA was observed during lactation. The proportion of polymeric and monomeric IgA in serum and milk was evaluated by gel exclusion chromatography. The onset of lactatin led to a rise in the proportion of polymeric IgA (P-IgA) in serum from 37% to 51%. The proportion of P-IgA in milk was 65% and remained constant throughout lactation. P-IgA and albumin were shown to be efficiently transferred from the serum of lactating mice into their milk. Serum decay studies were performed to evaluate the turnover of the serum pools during lactation. The rates of disappearance from the serum of isotopically labeled albumin and P-IgA were observed to increase dramatically during lactation, suggesting that both of these two mild proteins might be derived at least in part from the serum. The sites of synthesis of mild IgA (local vs. extra-mammary gland) were evaluated by determining the extent of dilution of isotopically labeled serum IgA during transport through the mammary gland into the milk. Early in lactation, the majority of the IgA in mouse milk appeared to be derived from distant sites and transferred via the blood to the mammary gland. However, by day 8 of lactation, the isotopically labeled P-IgA in milk was significantly diluted by the IgA synthesized in the mammary gland. Albumin and IgG were not diluted by local synthesis indicating that these proteins were exclusively serum-derived.

Animals↗
PubMed1997

Effect of aging on norepinephrine and phenylephrine stimulated lactate production by white adipocytes.

We have recently demonstrated that adipose tissue can produce lactate independently of lipolysis in insulin-resistant rats and that lactate production depends on alpha 1-adrenergic stimulation. In this study, we have investigated the influence of aging on norepinephrine-and-phenylephrine-stimulated lactate production and glycerol production. We showed that basal and norepinephrine stimulated lactate production were significantly increased in adipocytes isolated from old vs. young rats (0.165 +/- 0.006 vs. 0.055 +/- 0.008 for basal and 0.567 +/- 0.026 vs. 0.277 +/- 0.019 mumol lactate/10(6) cells/15 minutes for norepinephrine-stimulated lactate production, respectively, p < 0.05). The sensitivity of lactate production to norepinephrine stimulation in adipocytes isolated from old rats was significantly decreased (EC50 = 523 +/- 63.7 vs. 46.7 +/- 6.34 nM, respectively, p < 0.05). Maximal lactate production obtained with norepinephrine and phenylephrine was not significantly different in either group (0.567 +/- 0.026 vs. 0.520 +/- 0.036 in old and 0.277 +/9 0.019 vs. 0 275 +/- 0.017 mumol/10(6) cell/15 minutes in young rats, respectively, ns). Lactate production by adipocytes isolated from old rats were significantly less sensitive to phenylephrine stimulation compared with young (EC50 = 3.67 +/- 1.16 vs. 0.07 +/- 0.01 nM, respectively, p < 0.05) indicating that the effects of aging on norepinephrine and phenylephrine stimulation were probably induced by a decreased number of alpha 1-adrenoceptors. The mechanism by which aging increases adipocyte responsiveness of lactate production has not yet been elucidated.

Adipocytes↗