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PubMed1989

Cerebrospinal fluid/serum lactic acid in febrile convulsions.

Cerebrospinal fluid/serum lactic acid was prospectively assayed in 42 patients with febrile convulsions. Patients were divided into two groups for analytical purposes. Those with brief febrile seizures (30 patients) and the remaining 12 patients had prolonged febrile seizures. CSF and serum lactic acid values were within normal range in patients with brief seizures while elevated values were obtained in patients with prolonged seizures. The mean CSF lactic acid on admission was significantly higher (P less than 0.001) in patients with prolonged seizures than corresponding values in those with brief seizures. Mean serum lactic acid on admission was also significantly higher in patients with prolonged febrile seizures compared to the corresponding mean value in patients with brief seizures (P greater than 0.001). Patients who recovered with neurological deficits had significantly higher CSF lactic acid on admission (P greater than 0.001). Similarly 8 patients who had recurrent febrile convulsions had significantly higher CSF lactate on admission. It is suggested that measurement of CSF lactate can be used as a biochemical marker to identify children with prolonged seizures and those who are likely to have recurrent febrile seizures.

Biomarkers↗

PubMed1995

The effects of dichloroacetate on lactate accumulation and endurance in an exercising rat model.

Severe lactic acidosis usually accompanies intense endurance exercise. It has been postulated that glycogen depletion working in concert with elevated muscle and plasma lactate levels lead to a concomitant reduction in pH. Their cumulative effect during prolonged physical exertion now leads to muscular fatigue and eventually limit endurance capacity. Therefore in the present study, dichloroacetate (DCA), a compound which enhances the rate of pyruvate oxidation thus reducing lactate formation, has been evaluated in a validated rat model of sub-maximal exercise performance. Male rats (350 g) were divided into two groups (control-saline, i.v. and DCA 5 mg/kg, i.v.) and were exercised to exhaustion in a chamber (26 degrees C) on a treadmill (11 m/min, 6 degrees incline). When compared to controls, the DCA-treated rats had longer run times (169 vs 101 min) and a decreased heating rate (0.020 vs 0.029 degrees C/min). In addition, DCA attenuated the increase in plasma lactate (28 vs 40 mg/dl) and significantly reduced both the rate and absolute amount of depletion of muscle glycogen stores. These results suggest that the activation of pyruvate dehydrogenase activity by DCA resulted in a reduction in the rate of glycogenolysis in addition to decreasing lactate accumulation by presumably limiting the availability of pyruvate for conversion to lactate, therefore increasing muscle carbohydrate oxidation via the TCA cycle. Thus DCA effected a significant delay in muscle fatigue.

Acidosis, Lactic↗

PubMed1999

Identification of risk factors for delayed onset of lactation.

OBJECTIVE: To identify infant feeding, socioeconomic, demographic, and delivery-related factors that affect women's self-reported timing of the onset of lactation. DESIGN: Longitudinal survey of women from day 1 postpartum until self-reported onset of lactation. Subjects were interviewed in person on day 1 postpartum, then surveyed daily by telephone regarding infant feeding method, breast symptoms, and perception of whether the onset of lactation had occurred. Medical records were reviewed. SUBJECTS/SETTING: Data were collected from 192 women after they gave birth to a healthy, term singleton. STATISTICAL ANALYSES PERFORMED: chi 2 Analyses were used to identify variables associated with delayed onset of lactation (onset of lactation > or = 72 hours postpartum). Multivariate logistic regression was used to identify the independent association of each significant variable with delayed onset of lactation. RESULTS: Risk factors for delayed onset of lactation included white/Hispanic ethnicity, heavy/obese body build, delivery of offspring by unscheduled cesarean delivery, vaginal delivery with prolonged stage 2 labor, infant birth weight less than 8 lb, and exclusive formula-feeding before the onset of lactation. APPLICATIONS/CONCLUSIONS: Women who are at risk for delayed onset of lactation need additional breast-feeding support during the first week postpartum. During their hospitalization, these women should be instructed about the normal lactation process and the possibility that onset of lactation may occur later than 72 hours postpartum. Frequent nursing should be recommended, as delayed onset of lactation was associated with the lack of infant suckling.

Adult↗

PubMed1977

Actions of fenfluramine on glucose uptake in vitro and in vivo.

Fenfluramine stimulates the glucose uptake of the isolated hemidiaphragm from normal and streptozotocin diabetic rats in the presence of insulin. The drug does not cause an increased storage of glycogen. During hind leg perfusion of the dog fenfluramine stimulated peripheral glucose uptake. No increase in lactate or in free fatty acids release was observed during prolonged infusions of the drug. Fenfluramine caused an improvement of glucose tolerance in normal glucose-primed rats. A single dose of fenfluramine significantly lowered the blood glucose levels in streptozotocin diabetic rats and in diabetic dogs treated with insulin. Prolonged treatment with fenfluramine of streptozotocin diabetic rats had no significant effect on blood glucose levels. Additional treatment for one week of insulin dependent diabetic dogs with small non-anorexic doses of fenfluramine resulted in slightly decreased blood glucose levels. The dogs could not be maintained on fenfluramine alone (without insulin).

Animals↗

PubMed2004

Visual stimulation, 1H MR spectroscopy and fMRI of the human visual pathways.

The purpose was to assess changes in lactate content and other brain metabolites under visual stimulation in optical chiasm, optic radiations and occipital cortex using multiple voxel MR spectroscopy (MRS). 1H chemical shift imaging (CSI) examinations of transverse planes centered to include the above structures were performed in four subjects at an echo time of 135 ms. Functional MRI (fMRI) was used to confirm the presence of activity in the visual cortex during the visual stimulation. Spectral maps of optical chiasm were of poor quality due to field disturbances caused by nearby large blood vessels and/or eye movements. The optic radiations and the occipital lobe did not show any significant MR spectral change upon visual stimulation, i.e., the peak areas of inositol, choline, creatine, glutamate and N-acetylaspartate were not affected. Reproducible lactate signals were not observed. fMRI confirmed the presence of strong activations in stimulated visual cortex. Prolonged visual stimulation did not cause significant changes in MR spectra. Any signal observed near the 1.33 ppm resonance frequency of the lactate methyl-group was artifactual, originating from lipid signals from outside the volume of interest (VOI). Previous claims about changes in lactate levels in the visual cortex upon visual stimulation may have been based on such erroneous observations.

Adult↗

PubMedDate not supplied

[Possibilities for prolonging the maximal time for kidney ischemia in using different variants of anti-ischemic protection].

An antiischemic effect of kidney cooling to 16-18 or 4 degrees C, washing-up of the kidney with a cold preserving solution (Eurocollins solution) and medication (alpha-tocopherol as an oil solution or emulsion and isoptin) was studied in stopping renal blood flow for 1 to 24 hours in 94 white non-inbred rats. The damage was assessed during the organ reperfusion with oxygenized solution by the released intracellular lactate dehydrogenase and accumulated cortical malonic dialdehyde. Cooling of the kidney prolonged the time to marked alterations by 1 hour. Pretreatment with the drugs or addition of the drugs to the reperfusion solution prolonged permissible ischemia by 1 more hour in cooling to 16-18 degrees and 2 hours in cooling to 4 degrees C. Lavage of the kidney with the solution and cooling to 16-18 degrees C had no advantages over cooling alone while in cooling to 4 degrees C damage to cell metabolism intensified only after 6 hours of ischemia. The most prominent antiischemic effect was observed in combination of all three factors of antiischemic defense (cooling, preserving solution and medication).

Animals↗

PubMed1997

Carbohydrate handling in exercising muscle of obese Zucker rats.

OBJECTIVE: To determine the differential substrate utilization of substrates by exercising muscle and in the fatigued state in lean and obese rats. DESIGN: The rats were treadmill-exercised until fatigued, when their oxygen consumption increased by 1.85 x factor. Blood and hind leg tissue (muscle and skin) were sampled at intervals during exercise and recovery. SUBJECTS: Lean and obese adult Zucker female rats. MEASUREMENTS: Three series of rats were used to determine hind-leg glucose, lactate and oxygen arterio-venous balances, blood flow and muscle levels of glucose, hexose-P, glycogen, lactate and skin lactate. The rates of glycosyl unit flow during exercise and recovery were then calculated. RESULTS: In obese rats, exercising muscle showed higher glucose uptake, increased glycogen mobilization and lower lactate production than in the lean. In the obese rats' muscle, there were more glycosyl units available for oxidative metabolism. Excess glycosyl (or 3C) units were used probably for lipid synthesis. Lean rats managed their glycosyl units more efficiently, stretching the available glycogen, thus prolonging the exercise. During recovery, obese rats massively synthesized glycogen and lowered lactate efflux, which left only a few glycosyl units to oxidative metabolism; probably the rest of oxidative energy was derived from lipids. CONCLUSION: In lean rats glucose is the main source of muscle energy during exercise and recovery, whereas obese rats use glucose during exercise, and probably synthesize lipid during exercise. Obese rats rely more on lipids for energy during recovery.

Animals↗

PubMed1984

Effects of oestradiol benzoate treatment on the reproductive performance and endocrine status of sows after lactations of 10 or 35 days.

Forty-two Landrace X Large White sows were used in 3 studies of oestradiol benzoate treatment 24 h (E1) or 48 h (E2) after piglet removal, following lactations of 10 (S) or 35 (L) days, or were untreated controls (C). For Exp. 1, oestradiol benzoate doses were 4, 16 and 64 micrograms/kg body weight; since highest mean LH peaks followed use of the 16 micrograms/kg dose, this treatment was used in later studies. Treatments for Exp. 2 were S-E1 and L-E1 (N = 3). Pregnancy rates were 1/3 and 2/3, respectively, while 10-day weaned sows tended to have longer weaning-remating intervals, shorter oestrous periods and lower post-injection oestradiol peaks. Post-treatment LH peaks were recorded from all L-E1 sows, but only one S-E1 animal. Treatments S-E2, L-E2, S-C and L-C (N = 6) were used in Exp. 3; pregnancy rates were 1/6, 6/6, 5/6 and 6/6, respectively, while peak oestradiol levels were 49.5 +/- 8.3, 74.8 +/- 15.1, 21.7 +/- 2.0 and 51.8 +/- 26.5 pg/ml, respectively. Weaning-remating intervals were extended in S-C sows (P less than 0.05), while oestradiol treatment prolonged behavioural oestrus. LH peak values were reduced after short lactations, but not affected by oestradiol treatment. Plasma prolactin concentrations at weaning were higher in sows in treatment S than in treatment L, while at the subsequent oestrus in oestradiol-treated sows they were elevated more and for longer periods than in controls. These results demonstrate that reduced gonadotrophin secretion and fertility after short lactations are not overcome by treatment with oestradiol benzoate.

Animals↗

PubMed2004

Mice lacking alpha-synuclein have an attenuated loss of striatal dopamine following prolonged chronic MPTP administration.

The functional role of alpha-synuclein in the pathogenesis of Parkinson's disease (PD) is not fully understood. Systemic exposure of alpha-synuclein-deficient mice to neurotoxins provides a direct approach to evaluate how alpha-synuclein may mediate cell death in a common murine model of PD. To this end, wild-type and homozygous alpha-synuclein knock-out mice were treated with sub-chronic and prolonged, chronic exposure to 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP). In the sub-chronic model, wild-type and alpha-synuclein knock-out mice were treated for five consecutive days with MPTP (1-25 mg/kg, s.c.) or vehicle, and sacrificed 3 days following the last injection. The prolonged, chronic model consisted of two injections of MPTP (1-20 mg/kg, s.c.) per week for 5 weeks, with co-administration of probenecid (250 mg/kg, i.p.), and animals were sacrificed 3 weeks following the last injection. Sub-chronic administration of MPTP caused a dramatic, dose-dependent decrease in striatal dopamine (DA) concentrations, while an attenuated response was observed in alpha-synuclein knock-out mice. Similarly, prolonged, chronic administration of MPTP produced a dose-dependent decrease in striatal DA concentrations, and a corresponding loss of striatal vesicular monoamine transporter (VMAT-2) protein in wild-type mice. However, mice lacking alpha-synuclein had an attenuated loss of striatal DA concentrations, while no loss of striatal VMAT-2 protein was observed. Both sub-chronic and prolonged, chronic administration of MPTP caused an increase in the 3,4-dihydroxyphenylacetic acid (DOPAC) to DA ratio in wild-type mice, but not in mice lacking alpha-synuclein. Despite attenuated toxicity, elevated lactate concentrations were observed in alpha-synuclein knock-out mice following prolonged, chronic MPTP administration. The results of this study provide evidence that alpha-synuclein null mice have an attenuated response to the toxic effects of MPTP exposure, even over prolonged periods of time and that the biochemical sequela of a protracted insult to nigrostriatal DA neurons are distinct between mice with and without alpha-synuclein expression.

1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine↗

PubMed1998

Preconditioning human cardiomyocytes and endothelial cells.

BACKGROUND: The effects of simulated "ischemia" and "reperfusion" were evaluated in cell cultures of human ventricular cardiomyocytes and human saphenous vein endothelial cells. METHODS: Myocyte and endothelial cell cultures were exposed to a low volume (1.5 ml) of either hypoxic (oxygen tension = 16 mm Hg) or anoxic (oxygen tension = 0 mm Hg) phosphate-buffered saline solution for 90 minutes ("ischemia") followed by 30 minutes of simulated "reperfusion." Cell injury was evaluated by trypan blue exclusion. Next, the effects of a preconditioning stimulus were evaluated by a brief (10 minute) exposure to hypoxic or anoxic ischemia and 10 minutes of reperfusion before prolonged (90 minutes) anoxic ischemia. Finally, the effects of anoxic preconditioning on intracellular lactate accumulation and extracellular lactate and acid release were assessed. RESULTS: "Ischemia" and "reperfusion" resulted in greater injury to endothelial cells than to cardiomyocytes. In both cell types, anoxic ischemia resulted in greater injury than hypoxic ischemia. Preconditioning reduced cell injury in myocytes but not in endothelial cells. Endothelial cells produced more lactate than cardiomyocytes under normoxic conditions. Ischemia increased lactate accumulation and release in cardiomyocytes but not endothelial cells. Preconditioning reduced lactate accumulation and release in cardiomyocytes but not endothelial cells. CONCLUSIONS: Endothelial cells were more susceptible to the same period of simulated ischemia than cardiomyocytes. Preconditioning protected cardiomyocytes but not endothelial cells from a subsequent prolonged period of ischemia and reperfusion.

Cell Hypoxia↗

PubMed1995

Plasmodium berghei infection: dichloroacetate improves survival in rats with lactic acidosis.

The kinetics of Plasmodium berghei infection and the development of lactic acidosis, hypoglycemia, and anemia were defined in young Wistar rats. This model of metabolic dysfunction, which is similar to that of severe human malaria, was used to test the hypothesis that dichloroacetate, a treatment for lactic acidosis, prolonged survival in rats receiving a single antimalarial dose of quinine (20 mg/kg). Rats with hyperlactatemia (lactate > 5 mmol/liter, N = 183) were randomized to receive either dichloroacetate (100 mg/kg, N = 99) or saline (N = 84) and were monitored for outcome (survival or death) for 50 hr. Logistic regression modeling adjusting for baseline venous lactate concentration demonstrated that dichloroacetate increases survival rates in rats with venous lactate concentrations between 5 and 8.9 mmol/liter (odds ratio > 2.2, P < 0.021). This is the first demonstration that specific intervention to treat lactic acidosis can prolong survival and suggests that dichloroacetate may be useful as adjunctive therapy in the management of lactic acidosis complicating severe falciparum malaria.

Acidosis, Lactic↗

PubMed2005

Effects of hypothyroidism on mammary and liver lipid metabolism in virgin and late-pregnant rats.

Untreated maternal hypothyroidism (hypoT) has serious consequences in offspring development that may result from the effect on lactation of maternal metabolism dysfunction. We studied the effects of prolonged propylthiouracil (PTU)-induced hypoT (0.1% PTU in drinking water starting 8 days before mating until day 21 of pregnancy or for 30 days in virgin rats) on liver and mammary lipid metabolism and serum lipid concentrations. In virgins, hypoT reduced hepatic mRNAs associated with triglyceride (TG) and cholesterol synthesis (including fatty acid synthase and 3-hydroxy-3-methylglutaryl coenzyme A reductase), and induced lobuloalveolar mammary development. Pregnancy increased hepatic mRNAs associated with TG and cholesterol synthesis and uptake (including LDL receptor) and with lipid oxidation, such as acyl CoA oxidase. HypoT decreased mRNAs and the activity of proteins associated with TG synthesis, and mRNAs associated with cholesterol uptake and lipid oxidation. Pregnancy increased mammary mRNAs related to lipid oxidation and decreased cholesterol synthesis, whereas hypoT decreased mRNAs and activities of proteins associated with TG synthesis and decreased epithelial mammary tissue. Virgin and pregnant hypoT rats had increased circulating VLDL + LDL cholesterol. HypoT decreased circulating TGs in pregnant rats. The observed effects of hypoT may result in decreased mammary lipid availability. This, along with the decreased epithelial mammary tissue during lactogenesis, may contribute to the future lactational deficit of hypoT mothers.

Animals↗

PubMed1976

The fine structure of the interhemal membrane of the rat chorioallantoic placenta during prolonged pregnancy.

In placentas from viable rat fetuses which surgically had been retained beyond term in lactating animals for as long as four days, the fine structure of much of the interhemal membrane was quite like that of full-term placentas. Moreover, contrary to what has been reported previously (Jollie, '64a), in retained placentas which were autopsied at term there were few changes in the four cytoplasmic layers of the membrane which could be interpreted as degenerative. With prolongation of the placenta beyond normal delivery the number of pericytes which were associated with the allantoic endothelium increased; the basal lamina separating the endothelium from trophoblast III progressively became more focally split; and the apposed plasma membranes between this latter layer and trophoblast II appeared to dissociate. Trophoblast II became regionally divided in its cytoplasmic organization, its more superficial zone becoming highly infolded and/or vacuolar. As a consequence, the intertrophoblastic space between layers I and II became more extensive and complex. Within this space, a flocculent material appeared; and there was ultrastructural evidence of massive pinocytosis from the space by trophoblast II. With increased prolongation of gestation, a variety of lysosome-like inclusions appeared within this layer of the membrane.

Allantois↗

PubMed1999

The effect of bovine somatotropin (bST) administration on reproduction, progesterone concentration during lactation and LH secretion during estrus, in dairy ewes.

Twenty-two polytocous lactating Chios ewes were used to test the effects of bovine somatotropin (bST) on reproduction, progesterone concentration and LH secretion during estrus. Half of the ewes were injected every second week with 160 mg bST in a prolonged release vehicle, from the fifth day post partum until the end of lactation, while the remaining ones were used as controls. All animals were fed the same amount of ration. Supplementation with bST resulted in an increase of milk production (P<0.05) and an insignificant trend for delayed resumption of normal estrous cycles. Although there were no differences between groups, there was also a tendency for the bST group to display lower progesterone concentrations during the first three fortnights after the onset of normal estrous cycles and higher ones during the last three fortnights of the experiment, compared with the control group. Duration of the first normal luteal phase after delivery of the bST group was found to be shorter compared with the control group (P<0.05). After estrous synchronization the bST group showed a shorter estrus compared with the control group (P<0.05). Average and baseline LH concentrations during synchronized estrous in the bST group was lower (P<0.001) compared with the control group. Additionally, the conception rate did not differ between the two groups. This study supports the concept that the beneficial effects of bST treatment on milk production outweigh the potential deleterious effects on reproduction.

Animals↗

PubMed1993

Reliability, reproducibility and validity of the individual anaerobic threshold.

The individual anaerobic threshold (IAT) has been defined as the highest metabolic rate at which blood lactate (La) concentrations are maintained at a steady state during prolonged exercise. The validity of this definition, however, has not been substantiated. Eleven men [maximum oxygen uptake (VO2max), mean (SD), 57.8 (6.9) ml.kg-1 x min-1) did two maximal incremental cycle exercise tests (30 W and 4 min per step). Blood was sampled repeatedly during exercise and for 9 min during the subsequent recovery period with light activity. The subjects then exercised at the power output equivalent of IAT for 45 min, until they could no longer continue or until rectal temperature reached 39 degrees C. Subjects performed two additional exercise tests. The intensity of these tests depended upon the LA and acid-base responses during the last 15 min of at least 30 min of exercise at IAT. If a steady state was achieved (La, pH and PCO2 changed by less than 0.5 mmol.l-1, 0.005 pH units and 0.3 kPa, respectively) or decreasing La and increasing pH values were observed, then the second test was performed at IAT +5% VO2max and the third session at either IAT +2.5% or +7.5% VO2max. Conversely if a steady state was not achieved during exercise at the calculated IAT, the intensity of the second test was set at IAT -5% VO2max. Depending on the La and acid-base responses during this test, the final session was performed at either IAT -2.5% or -7.5% VO2max.(ABSTRACT TRUNCATED AT 250 WORDS)

Acid-Base Equilibrium↗

PubMed1989

Active recovery, endurance training, and the calculation of the individual anaerobic threshold.

The individual anaerobic threshold (IAT) is the highest metabolic rate at which blood lactate (LA) concentrations are maintained at a steady state during prolonged exercise. The purpose of this study was to compare the effects of active and passive recovery on the determination of the IAT before and after an endurance training program. Both before and after an 8-wk training program, nine subjects did two submaximal, incremental cycle exercise tests (30 W and 4 min per step) until LA was greater than or equal to 4 mmol.l-1. Blood was sampled repeatedly during exercise and for 12 min during the subsequent recovery period, which was passive for one test and active (approximately 35% VO2max) during the second test. An IAT metabolic rate and power output were calculated for the passive (IATp) and active (IATa) recovery protocols. On separate days, before and after training, five of the subjects exercised for 30 min at either the IATp or the IATa. Before training, IATa occurred at a higher (P less than 0.05) power output and absolute and relative VO2 compared to IATp. After training, VO2max and the power output and VO2 at IATa and IATp increased significantly; as a percent VO2max, IATp but not IATa increased. During the pretraining 30-min IAT rides, LA was higher during the IATa than the IATp test, but LA values did not change during the last 20 min of exercise. LA was similar for both 30-min IAT rides after training and did not change from 5 to 30 min of exercise. The LA steady-state concentrations ranged from 1.3 to 6.8 mmol.l-1.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMed1975

Effects of coronary hypotension on myocardial substrate utilization.

Changes in myocardial substrate utilization were studied after experimental coronary hypotension in the isolated dog heart perfused with the blood of a large donor animal. After a control period (100 mmHg) the afterload of the isolated heart was adjusted to 50 mmHg and kept at that level for 4 h. After this period, a second control observation was made at a 100-mmHg afterload. Coronary sinus blood flow and oxygen consumption decreased during hypotension and returned to normal during the second control period. Myocardial free fatty acid (FFA) uptake and oxidation did not change significantly. Lactate uptake and the percentage of CO2 derived from myocardial lactate utilization were both diminished during hypotension. These changes were not present during the second control period. Glucose uptake and myocardial respiratory quotient were decreased during the hypotensive period. Half the hearts exhibited elevated end-diastolic pressure after hypotension, but no metabolic differences were detectable between the failing and nonfailing hearts. Thus, prolonged severe hypotension caused a relative preference of FFA oxidation and diminished lactate and glucose uptakes by the myocardium. These changes were quite different from those obtained during experimental hemorrhagic or endotoxic shock.

Animals↗

PubMed1990

Effect of THAM on brain oedema in experimental brain injury.

The metabolic brain acidosis after trauma has been thought to increase brain oedema and contribute to neurologic deterioration. Amelioration of the brain acidosis either by systemic buffering agents or by hyperventilation has been proposed as a method of treatment. The objective of this study was to explore brain oedema and the metabolic changes in brain that occur with the use of hyperventilation. Tromethamine and combination (THAM and hyperventilation) therapy in experimental fluid-percussion brain injury. Brain lactate, brain pH, inorganic phosphate (Pi) and ATP were measured by 1H and 31P magnetic resonance spectroscopy. Also Water content in brain tissue using the specific gravimetric technique were determined in 32 cats. Prolonged hyperventilation provided relative ischaemia in brain tissue and promoted more production of brain lactate, no recovery of PCr/Pi ratio, and no decrease in brain oedema. On the other hand the administration of THAM served to decrease production of brain lactate and brain oedema and promoted the recovery of cerebral energy dysfunction. THAM ameliorates the deleterious effects of hyperventilation by minimizing energy disturbance and also decreases brain oedema. We conclude that THAM may be effective in reducing brain tissue acidosis and helpful as a metabolic stabilizing agent following severe head injury.

Animals↗