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PubMed1983

Respiratory gas analysis during exercise as a noninvasive measure of lactate concentration in chronic congestive heart failure.

Measurement of blood lactate during exercise in patients with chronic congestive heart failure provides a useful index of oxygen (O2) availability in working muscle. Bicarbonate buffering of lactate produces carbon dioxide (CO2) in excess of that resulting from oxidative metabolism. Therefore, calculation of excess CO2 production from measured CO2 production and O2 uptake may offer a noninvasive quantitative index of changes in blood lactate during exercise in these patients. To investigate this possibility, 22 patients with congestive heart failure and depressed left ventricular function were studied during progressive maximal upright bicycle exercise. Oxygen uptake, expired carbon dioxide, arterial lactate, O2 extraction, and cardiac output were measured at each 20 W incremental work load and peak exercise. Exercise increased VO2 from 3.5 +/- 0.9 ml/min/kg at rest to 13.1 +/- 2.9 ml/min/kg, O2 extraction from 49 +/- 9% at rest to 78 +/- 6%, lactate from 12 +/- 5 mg/dl at rest to 41 +/- 15 mg/dl, and cardiac index from 1.7 +/- 0.4 at rest to 3.8 +/- 1.2 liters/min/m2. The increase in lactate at each work load was linearly related to excess CO2 production (r = 0.92, p less than 0.01). Exercise was repeated the following day in 10 patients; measurements of excess CO2 production was highly reproducible (r = 0.98, p less than 0.01). Excess CO2 production also correlated with the decrease in bicarbonate produced by exercise (r = 0.81), supporting the hypothesis that excess CO2 is produced by bicarbonate buffering of lactate. Thus, calculation of excess carbon dioxide production from noninvasive measurement of respiratory gas exchange provides a reliable and reproducible method of continuously assessing alterations in lactate throughout bicycle exercise in patients with chronic congestive heart failure.

Bicarbonates↗
PubMed1985

Serum lactate dehydrogenase levels in adults and children with acquired immune deficiency syndrome (AIDS) and AIDS-related complex: possible indicator of B cell lymphoproliferation and disease activity. Effect of intravenous gammaglobulin on enzyme levels.

Twenty-seven of 33 patients with the acquired immune deficiency syndrome (AIDS) or AIDS-related complex (16 adults and 17 children) demonstrated significant elevation of serum lactate dehydrogenase activity, occurring in the isomorphic distribution. Serum lactate dehydrogenase activity was the highest in all nine patients with acute Pneumocystis carinii pneumonitis, in seven of whom extensive interstitial pulmonary infiltrates with lymphocytes and plasma cells were documented. Lactate dehydrogenase activity was also significantly elevated on a long-term basis in all 17 pediatric patients with non-Pneumocystis lymphoid interstitial pneumonitis. Clinical resolution of Pneumocystis carinii pneumonitis was associated with a decline in lactate dehydrogenase activity. Periodic intravenous gammaglobulin was more effective than conventional therapy (trimethoprim/sulfamethoxazole and pentamidine) in achieving clinical and immunologic improvement and reduction of serum lactate dehydrogenase activity in patients with Pneumocystis carinii pneumonitis. Intravenous gammaglobulin was also more effective in patients with AIDS and non-Pneumocystis carinii pneumonitis and lymphoid interstitial pneumonitis. Lactate dehydrogenase activity declined to normal, at least temporarily, in nine of 12 intravenous gammaglobulin-treated patients as compared with only two of 12 untreated patients. Six adult patients with AIDS or AIDS-related complex and no interstitial pneumonitis exhibited normal lactate dehydrogenase levels. These findings suggest that serum lactate dehydrogenase activity in patients with AIDS or AIDS-related complex may be a useful indicator of pulmonary interstitial inflammation. As such, it may be utilized to predict disease course and monitor response to intravenous gammaglobulin treatment.

Acquired Immunodeficiency Syndrome↗
PubMed1985

Some factors affecting the diffusion of [14C]-lactate in human dental plaque.

The apparent diffusion rate, D, of lactate was significantly retarded in dental plaque fluid and a simulated plaque fluid consisting of a chemically-defined solution of salts, amino acids and albumin in phosphate buffer at pH 6.5. Metabolic utilization of lactate in live plaque residue reduced D for lactate into such samples of residue, compared with killed samples. D in plaque residue was lower than in a previous study. Increasing the packing density of killed plaque residue of Streptococcus sanguis cells reduced D. Pre-incubation of plaque residue with sucrose or sucrose + NaF reduced D for lactate. No such relationship was found when Streptococcus mutans was so treated, but D for lactate was lower when the cells were grown in tryptone-soy broth supplemented with 5 per cent sucrose compared with unsupplemented broth. The retardation of lactate increased with an increase in ion-exchange capacity of cation- and anion-exchange Sephadex gel-model systems. Thus, the apparent diffusion coefficient of lactate in dental-plaque residue is influenced by the chemical composition of the plaque aqueous phase, by metabolism of lactate, by plaque tortuosity, sucrose metabolism and ion-exchange interactions.

Dental Plaque↗
PubMed1977

Kinetic formulations for the oxidation and the reduction of glyoxylate by lactate dehydrogenase.

Chicken liver lactate dehydrogenase (L-lactate : NAD+ oxidoreductase, EC 1.1.1.27) irreversibly catalyses the oxidation of glyoxylate (hydrated form) (I) to oxalate (pH = 9.6) and the reduction of (non-hydrated form) (II) to glycolate (pH = 7.4). (I) attaches to the enzyme in the pyruvate binding site and (II) attaches to the enzyme at the L-lactate binding site. The oxidation of (I) (pH = 9.6) is adapted to the following mechanism: (see book). The abortive complexes, E-NADH-I and E-NAD+-II, are responsible for the inhibition by excess substrate in the reduction and oxidation systems, respectively. When lactate dehydrogenase and NAD+ are preincubated, E-NAD+- NAD+ appears and causes inhibition by excess NAD+ in the glyoxylate-lactate dehydrogenase-NAD+ and L-lactate-lactate dehydrogenase-NAD+ systems; the second NAD+ molecule attaches to the enzyme at the L-lactate binding site.

Animals↗
PubMed1994

Analysis of p-nitrophenol glucuronidation in hepatic microsomes from lactating rats.

In the present study, hepatic p-nitrophenol glucuronidation was analyzed comparatively in virgin female, lactating mother and nonlactating mother rats (the last two groups 19-21 days post-partum). Enzyme assays were performed in native and activated microsomal suspensions. Activation was achieved either by including UDP-N-acetylglucosamine in the incubation mixtures or by preincubating native microsomes with optimal concentrations of Triton X-100 or palmitoyl-lysophosphatidylcholine. When UDP-N-acetylglucosamine was used as activator, enzyme activity increased in both lactating (about 80% increment) and nonlactating mothers (about 30% increment) as compared with virgin females. From an analysis of the degree of activation by Triton X-100 and palmitoyl-lysophosphatidylcholine, it can be inferred that the pregnancy-delivery event decreased the latency of UDP-glucuronosyltransferase activity that was detectable even 3 weeks post-partum, irrespective of whether suckling newborns were or were not kept with their mothers (lactating and nonlactating mothers, respectively). The estimation of apparent Vmax toward UDP-glucuronic acid in palmitoyl-lysophosphatidylcholine-activated microsomes, which allows an estimation of the amount of the enzyme, showed that lactation increased the number of catalytic units (about 40%). Hepatic UDP-glucuronic acid content was 70% higher in lactating rats than in other groups. The lipid composition and membrane fluidity (using 1,6-diphenyl-1,3,5-hexatriene as probe) were also analyzed in microsomes from all groups. A significant decrease in the unsaturation index that correlated with the rigidization of microsomal membranes was consistent with the changes in the degree of enzyme latency observed in lactating and nonlactating mothers. In conclusion, lactating rats exhibited enhanced p-nitrophenol UDP-glucuronosyltransferase activity as well as an increase in the hepatic content of UDP-glucuronic acid. These findings and the fact that lactation increased the liver to body weight ratio emphasize the role of the liver in the metabolism of planar phenolic derivatives in these circumstances.

Animals↗
PubMed1989

Differential reactivity to lactate infusions: the relative role of biological, psychological, and conditioning variables.

Nine patients with panic disorder experienced a lactate-induced panic attack, whereas nine controls did not. Higher preinfusion anxiety levels and heart rates were associated with panic disorder, and high baseline anxiety ratings were associated with atypical, severe lactate-induced panic attacks. Nevertheless, it was difficult to reconcile patients' and controls' reactivity to lactate as entirely secondary to baseline differences. Subjects differed qualitatively in the types of specific symptoms experienced and quantitatively in their anxiety and heart rate responses. In most cases, panic began with various central perceptual changes; peripheral cardiovascular and autonomic symptoms followed later. No patient rated a lactate-induced panic attack as identical to a naturally occurring attack. Not only did specific symptoms differ in their severity and order of production, but lactate-induced panic lacked the typical fears of dying, going crazy, or losing control. The results suggest that though environmental effects, expectancy biases, and baseline psychological states play salient roles in modifying the experience of a lactate-induced panic attack, they do not fully account for lactate sensitivity. The relative role that biological, psychological, and conditioning factors play in lactate-induced panic is discussed.

Adult↗
PubMed1988

Morphine does not stimulate prolactin release during lactation.

The ability of morphine to stimulate prolactin and growth hormone (GH) release was investigated in male rats and in female rats during diestrus, proestrus and lactation. In agreement with previous reports, acute morphine administration produced an increase in circulating levels of prolactin in male and in diestrous and proestrous female rats. In contrast to these results, morphine administration (10 or 15 mg/kg, s.c.; 5 mg/kg, i.v.; 5 or 10 micrograms, i.c.v.) did not produce an increase in prolactin levels in lactating dams. Morphine stimulates prolactin release in part by decreasing dopamine turnover in the tuberoinfundibular neurons in the median eminence. In order to assess the functional activity of these neurons during lactation, haloperidol (0.1 or 0.5 mg/kg, i.v.) was given to lactating dams. There was a significant increase in prolactin levels following haloperidol administration, suggesting that these dopaminergic neurons are participating in the modulation of prolactin release during lactation. In contrast to the insensitivity of the lactating rat to morphine stimulation of prolactin release, the intraventricular administration of two other opiate receptor agonists, beta-endorphin (10 or 20 micrograms) and [D-Ala-D-Leu]enkephalin (DADLE; 5 or 10 micrograms), produced significant increases in circulating levels of this hormone. The GH response to morphine, beta-endorphin and DADLE was also measured in these same rats. All these opiate receptor agonists stimulated GH release in male rats and in female rats during diestrus and proestrus as well as during lactation. These observations suggest that the suckling stimulus during lactation renders the rat refractory to morphine stimulation of prolactin release, possibly as a result of down-regulation of the mu-opiate receptor subtype.

Animals↗
PubMed1993

Lactate mimics only some effects of D-glucose on epileptic depolarization and long-term synaptic failure.

Lactate supports normal synaptic function and may be neuroprotective following an anoxic insult. The present study investigated the effects of lactate on epileptic depolarization and long-term synaptic failure during a zero-magnesium-induced epileptic insult using the hippocampal slice preparation. In artificial cerebrospinal fluid (aCSF) containing 10 mM D-glucose, no epileptic depolarization was observed. At lower concentrations of D-glucose, epileptic depolarization occurred and often was followed by long-term synaptic failure. Low concentrations of lactate, in place of D-glucose, supported normal synaptic transmission. However, no concentration of lactate tested (up to 30 mM) blocked the occurrence of epileptic depolarization. High concentrations of lactate allowed for partial recovery of synaptic responses following epileptic depolarization. Reinstatement of D-glucose was necessary to observe this recovery. The results confirm that lactate can replace D-glucose in maintaining synaptic responses, but demonstrate that lactate cannot replace D-glucose in blocking an insult-induced depolarization. The inability of lactate to mimic all the effects of D-glucose is consistent with the notion of compartmentation of energy utilization within neurons.

Animals↗
PubMed1993

Glycogen in astrocytes: possible function as lactate supply for neighboring cells.

In order to contribute to the elucidation of the function of astrocyte glycogen in brain, studies on the fate of the glucosyl residues of glycogen were carried out on astroglia-rich primary cultures derived from the brains of newborn rats. On glucose deprivation astroglial cells rapidly deplete their glycogen. In contrast to the situation with hepatocytes, only lactate, but not glucose, is detectable in the medium surrounding the astroglial cells. Besides glucose, astroglial cultures can also use mannose as a substrate for the synthesis of glycogen and the generation of lactate. Although mannose-fed astroglial cells contain glucose-6-phosphate, they do not release a measurable amount of glucose into the culture medium. Instead of glucose the astroglial cells release high amounts of lactate into the culture medium. Gluconolactone or 2-deoxyglucose which prevent glycogen breakdown in astroglial cells after glucose deprivation, allow to discriminate between lactate generated from glycogen and lactate from other sources. The amount of lactate found in the medium in the absence of gluconolactone (or 2-deoxyglucose) exceeds the amount found in the presence of either compound by the lactate equivalents calculated to be contained in the cellular glycogen. In conclusion, glycogen in astrocytes can be considered as a store for lactate rather than for glucose.

Animals↗
PubMed1983

The effect of combined oral contraceptive steroids on the gonadotropin responses to LH-RH in lactating women with regular menstrual cycles resumed.

The effect of combined oral contraceptive steroids upon pituitary response to stimulation with 100 micrograms LH-RH was studied in both non-puerperal and lactating women with regular menstrual cycles. Serum prolactin concentration was 14.20 ng/ml in non-puerperal women whereas it was 39.37 ng/ml in lactating women. A comparability was shown in the LH response to LH-RH in non-puerperal women and lactating women. FSH response to LH-RH, however, was significantly exaggerated in lactating-menstruating women as compared to that of non-puerperal women. Combined oral contraceptive steroids lowered basal levels of LH and FSH in non-puerperal women and lactating women although the difference was not statistically significant in non-puerperal women. The LH and FSH maximal responses to LH-RH were significantly diminished in both non-puerperal and lactating women on combined oral contraceptives. There was, however, no difference in the mean LH or FSH responses between non-puerperal women and lactating women. Combined oral contraceptive steroids used in this study seemed to suppress ovulation by decreasing the pituitary responsiveness to LH-RH in lactating-menstruating women as well as in normally menstruating women.

Contraceptives, Oral↗
PubMed1984

Lipogenesis from U14C lactate in obese Zucker rat hepatocytes. Effect of albumin-bound oleate.

Lipogenesis from U(14C) lactate was studied in hepatocytes isolated from obese Zucker rats (fa/fa) their lean littermates (Fa/?) and Sprague Dawley rats. The distribution of radioactive carbon between the glycerol and the fatty acid moieties of the acylglycerols were studied. Radioactive lactate was better utilized for glycerol formation than it was for fatty acid formation in the obese rats. However, when oleate was added to the hepatocytic incubation medium, radioactive lactate was preferentially incorporated into the fatty acid moiety of the acylglycerols. Zucker obesity classified as a "metabolic obesity" by Meyer (1) depends upon abnormalities in carbohydrate metabolism associated with increased lipogenesis. This might be explained by biochemical shifts in the utilization of nutrients (2). Among the nutrients, lactate seems to be a better source of carbon than glucose for lipid synthesis (3). It has been shown that there is an increased hepatic portal blood concentration of lactate several hours after eating: about 4 mM in Wistar rats (4) and 10-15 mM in obese Zucker rats (3). We are interested in determinating the incorporation of carbon from lactate either into glycerol or into fatty acyl moieties of hepatic acylglycerols, and in determining the influence of exogenous fatty acids on acylglycerol synthesis, since a high level of circulating fatty acids in Zucker obese rats has been reported (5). Our purpose was to determine the incorporation of lactate into glycerol and fatty acyl moieties of acylglycerols, under the influence of oleate. Hepatocytes were isolated from ad libitum fed obese Zucker rats (fa/fa), their lean littermates (Fa/?) and Sprague-Dawley rats (SD). Incorporation of lactate was studied for three hours, in order to exclude short-term regulation effects and to allow oleate to be distributed into all cellular compartments.

Albumins↗
PubMed1989

Follicle-stimulating hormone-induced lactate secretion by cultured Sertoli cells does not require extracellular calcium.

Sertoli cells of the testis secrete lactate in response to follicle-stimulating hormone (FSH). It is thought that the developing germ cells use lactate as an energy substrate preferentially over glucose. However, the biochemical mechanism(s) involved in the regulation of lactate secretion in response to FSH are unknown. The purpose of this study was to determine if extracellular calcium was important for the actions of FSH during this response. It was found that the FSH-induced increase in lactate production by Sertoli cells was not dependent upon the presence of extracellular calcium. However, A23187 (a calcium ionophore) stimulated lactate secretion in the presence of extracellular calcium. When FSH and A23187 were tested together at maximal concentrations, more lactate was secreted than when either FSH or A23187 was tested alone. Neither verapamil, nifedipine nor diltiazem (calcium channel "blockers") were able to inhibit the ability of FSH to increase lactate secretion. These results indicate that FSH-induced secretion of lactate by cultured Sertoli cells is not dependent upon extracellular calcium.

Animals↗
PubMed1995

Attenuation of the magnitude of suckling-induced prolactin release with advancing lactation: mechanisms.

To study why suckling-induced plasma prolactin levels decline in magnitude with advancing lactation, we examined prolactin release in lactating rats following suckling and pharmacologic manipulations during early, mid- and late lactation. On day 2 of lactation, litters were adjusted to 8 pups. On day 3, dams were implanted with an atrial catheter and experiments were conducted on lactation days 5, 11 and 17. To examine suckling-induced prolactin release, pups were removed at 0800 h, an extension was attached to the catheter at 1100 h, and pups returned to dams at 1200 h. Blood samples were obtained before, and at 10, 30, 60, 90 and 120 min after suckling started. Prolactin responses to sulpiride and thyrotropin releasing hormone (TRH) administration were studied in lactating rats separated from their litters for 4 hours. Blood samples were obtained before, and at 10, 30, 60 and 90 min after sulpiride (10 or 40 micrograms/kg BW) and 5, 10, 20 and 30 min after TRH (1 or 4 micrograms/kg BW) in rats pretreated with sulpiride. Prolactin release in response to suckling, administration of sulpiride or sulpiride and TRH diminished as lactation advanced. From these results, we conclude that refractoriness in anterior pituitary lactrotropes to prolactin-releasing stimuli is at least partially responsible for the decline in suckling-induced prolactin release with advancing lactation.

Animals↗
PubMed1994

CNS regulation of blood lactate concentration in anesthetized rats.

This study evaluated the effect of stimulating the central nervous system (CNS) with neostigmine, an inhibitor of acetylcholinesterase, on the blood lactate concentration in fed rats and in rats fasted for 48 hours. After the rat was anesthetized with pentobarbital, neostigmine was stereotaxically injected into the third cerebral ventricle. In fed rats, the central injection of neostigmine significantly increased the blood lactate level, while concomitantly increasing plasma glucagon, epinephrine and norepinephrine concentrations. Constant infusion of somatostatin throughout the experiments, to inhibit glucagon secretion from the pancreas, did not affect alterations in blood lactate by central injection of neostigmine. In adreno-medullated rats, CNS-stimulation by neostigmine still increased plasma norepinephrine significantly, however, the alteration in blood lactate was only one-third of that in intact rats. Intraperitoneal propranolol, but not phentolamine, prevented the rise in lactate. Neostigmine increased lactate in fasted rats as well as in fed rats. We conclude that in anesthetized rats, stimulation of the CNS by neostigmine increases blood lactate mainly through circulating epinephrine and partially through circulating norepinephrine or direct sympathetic nervous stimulation; glucagon does not appear to be involved in the increase in blood lactate.

Anesthesia, General↗
PubMed1995

Increased serum D-lactate associated with diabetic ketoacidosis.

We hypothesized that serum D-lactate may be increased in vivo in diabetes mellitus as a result of increased glucose flux through the glyoxalase pathway and/or via hepatic ketone metabolism. Levels of D-lactate and related metabolic intermediates were measured in 30 cats with spontaneous diabetes mellitus and in one ketoacidotic nondiabetic cat. Serum D-lactate was significantly (P = .0051) elevated in cats with ketoacidosis (337.2 +/- 70.2 mumol/L) as compared with nonketoacidotic diabetic (140.3 +/- 58.8) and control (25.0 + 6.5) cats. Two nonketoacidotic cats also had high levels of D-lactate. There was a significant linear correlation (r = .684, P = .0001) between D-lactate and beta-hydroxybutyrate concentrations. Serum D-lactate did not correlate with serum glucose (r = .078, P = .6825), and in vitro erythrocyte D-lactate formation did not increase in the presence of hyperglycemia. These data suggest that hepatic ketone metabolism, rather than hyperglycemia, may be a major source of serum D-lactate in diabetics.

3-Hydroxybutyric Acid↗
PubMed1983

The effects of lactation and ambient temperature on the body temperature of female Norway rats.

Norway rat dams were placed in an ambient temperature of 4 degrees C, 22 degrees C, or 28 degrees C. Body temperatures were recorded over a two hour period on three days; each female was observed on Day 4 and Day 10 of lactation and three days after lactation was stopped. Body temperatures were initially higher during lactation than after lactation had stopped. Dams were less able to maintain their body temperatures in the 28 degrees C ambience on Day 4 of lactation than after lactation, and on Day 10 of lactation, were even less able to maintain their body temperatures than on Day 4. During lactation, dams were able to maintain and even increase their body temperatures in the 4 degrees C ambience. The data support the hypothesis that the acute hyperthermia encountered by rat dams during contact with their litters may be due to a physical restriction on maternal heat loss.

Animals↗
PubMed1989

Factors influencing the self-selection of calcium in lactating rats.

The effect of varying litter size and preventing milk delivery on the self-selection of calcium in lactating rats was assessed in two experiments. In Experiment 1, two groups of lactating rats, one having a litter size adjusted to four pups (n = 10) on the day after parturition and the other a litter size adjusted to 16 pups (n = 9), were given ad lib access to a 2.4% solution of calcium lactate, demineralised water, and a calcium deficient diet. Calcium, water and food intake were compared for these two groups both before impregnation and during 16 days of lactation. Females nursing 16 pups increased their calcium and food intake over the course of lactation more than did mothers nursing four pups. In Experiment 2, female rats were divided into four groups consisting of 10 nonimpregnated, 10 impregnated, 10 impregnated galactophore-cut, and nine sham-operated impregnated animals. To maintain pup health, and thus equivalent suckling stimulation among groups, litters of 8 pups were switched between galactophore-cut, impregnated and colony foster mothers every twelve hours. Over the course of lactation galactophore-cut dams showed an increase in calcium intake compared to nonlactating females and further, took in similar quantities of calcium to both intact and sham-operated impregnated animals in the first week of lactation. These studies showed that female rats do selectively increase their calcium intake during lactation. Moreover, this increase varies as a function of litter size and persists in the absence of milk delivery.

Animals↗
PubMed1993

The caloric demand of lactation does not alter spontaneous meal patterns, nutrient intakes, or moods of women.

The regulation of food and fluid intake in lactating women was examined by comparing maternal intake during lactation, 6 weeks postpartum, to intake in two groups of nonpregnant, nonlactating women. All subjects completed a questionnaire and then filled out a food-intake diary for seven consecutive days. Lactating women did not differ from body weight-matched, nonlactating controls in their total daily intakes or their meal patterns. However, they consumed a significantly smaller percentage of the recommended dietary allowances (RDA) per day than did their nonlactating counterparts. Lactating women were also significantly more calm both pre- and postmeal than were either of the control groups. These results indicate that the lactating women, at 6 weeks postpartum, did not increase their intake to compensate for the caloric demands of lactation. This may indicate that the lactating women catabolize weight gained during pregnancy faster than accounted for in the RDA, or that lactating women increase their metabolic efficiency.

Adult↗