Artykuły w czasopismach na temat „Plasma lactate concentration”
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Raum, M., D. Rixen, R. Linker, S. Gregor, B. Holzgraefe i E. Neugebauer. "Influence of Lactate Infusion Solutions on the Plasma Lactate Concentration". ains · Anästhesiologie · Intensivmedizin · Notfallmedizin · Schmerztherapie 37, nr 6 (czerwiec 2002): 356–58. http://dx.doi.org/10.1055/s-2002-32241.
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Davidson, D. Fraser. "Observations on the Relationships between Plasma Free Fatty Acids, Ketones and Bicarbonate in Acute Hyperglycaemia". Annals of Clinical Biochemistry: International Journal of Laboratory Medicine 34, nr 3 (maj 1997): 303–10. http://dx.doi.org/10.1177/000456329703400313.
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Some of the initial biochemical findings, obtained from 141 randomly-selected cases of acute hyperglycaemia (admission plasma glucose >20 mmol/L) were examined. When viewed in terms of their initial plasma bicarbonate concentration, three groups were identifiable. Plasma concentrations of free fatty acids (FFA), acetone and the sum of 3-hydroxybutyrate (3OHB) and lactate were different between these groups. However, there were no differences in plasma glucose or lactate concentrations. It was further observed that the relationship between the plasma FFA/albumin molar ratio, and ketone concentration could be described by a rectangular hyperbola, and the initial anion gap was linearly related to the sum of the 3OHB and lactate concentrations.
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LINDNER, A. "Measurement of plasma lactate concentration with Accusport". Equine Veterinary Journal 28, nr 5 (wrzesień 1996): 403–5. http://dx.doi.org/10.1111/j.2042-3306.1996.tb03112.x.
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Hutchesson, Andrew, Mary Anne Preece, George Gray i Anne Green. "Measurement of lactate in cerebrospinal fluid in investigation of inherited metabolic disease". Clinical Chemistry 43, nr 1 (1.01.1997): 158–61. http://dx.doi.org/10.1093/clinchem/43.1.158.
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Abstract Measurement of lactate concentrations in cerebrospinal fluid (CSF) has been suggested as part of the investigation of inborn errors of the electron transport chain, but little information exists regarding the reference range in children or the relationship between CSF and plasma concentrations. In 39 children without bacterial meningitis, diabetes, or recent seizures, we determined that the median (range) lactate concentrations in CSF and plasma collected concurrently were 1.4 (0.8–2.2) and 1.5 (0.6–2.3) mmol/L; the regression equation was CSF lactate = (0.38 ± 0.06) plasma lactate + 0.83 (r2 = 0.14). In 8 of 11 (73%) children with electron transport chain defects, CSF lactate was ≥3.0 mmol/L; however, 2 of these 8 had a normal plasma lactate concentration. CSF lactate was also increased in 2 children with nonketotic hyperglycinemia. The finding that CSF lactate concentrations may be increased despite a normal plasma lactate value in children with electron transport chain defects is an important clue to the diagnosis of these disorders.
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Stallknecht, Bente, Joop Madsen, Henrik Galbo i Jens Bülow. "Evaluation of the microdialysis technique in the dog fat pad". American Journal of Physiology-Endocrinology and Metabolism 276, nr 3 (1.03.1999): E588—E595. http://dx.doi.org/10.1152/ajpendo.1999.276.3.e588.
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In the present study the microdialysis technique was evaluated in an isolated autoperfused dog fat pad. Concentrations of glucose, lactate, and glycerol were measured in interstitial fluid by microdialysis and simultaneously in arterial and adipose venous plasma. Adipose tissue blood flow was measured by both133Xe washout and timed weighing of venous blood. Metabolite concentrations in adipose venous plasma calculated from interstitial and arterial metabolite concentrations and133Xe washout were positively correlated with measured venous concentrations (glucose: r = 0.95, lactate: r = 0.92, glycerol: r = 0.81). Calculated and measured venous plasma concentrations did not differ for either glucose or lactate, but for glycerol, calculated concentration was on average 76% of measured concentration. Metabolite exchanges (Fick’s principle) calculated from interstitial metabolite concentrations were positively correlated with measured exchanges only for lactate ( r = 0.69). In conclusion, metabolite concentrations in adipose venous plasma can be calculated from microdialysis measurements with greater accuracy for glucose and lactate than for glycerol. The precision, however, is too low to allow calculation of metabolite exchange when arteriovenous metabolite differences are low.
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Bovens, A. M. P. M., M. A. van Baak, J. C. P. M. Vrencken, J. A. C. Wijnen i F. T. J. Verstappen. "90 GENDER DIFFERENCE IN PEAK PLASMA LACTATE CONCENTRATION". Medicine & Science in Sports & Exercise 22, nr 2 (kwiecień 1990): S15. http://dx.doi.org/10.1249/00005768-199004000-00090.
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Zander, R., i D. J. Cooper. "Association between plasma ionized calcium and lactate concentration". Intensive Care Medicine 19, nr 6 (czerwiec 1993): 362–63. http://dx.doi.org/10.1007/bf01694716.
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Carraro, F., S. Klein, J. I. Rosenblatt i R. R. Wolfe. "Effect of dichloroacetate on lactate concentration in exercising humans". Journal of Applied Physiology 66, nr 2 (1.02.1989): 591–97. http://dx.doi.org/10.1152/jappl.1989.66.2.591.
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The precise mechanism responsible for the increase in plasma lactate concentration during exercise in humans is not known. We have used dichloroacetate to test the hypothesis that a limitation in pyruvate dehydrogenase activity is responsible for the rise in plasma lactate. Dichloroacetate stimulates the activity of pyruvate dehydrogenase, which is normally the regulatory enzyme in the oxidation of glucose when tissue oxygenation is adequate. Six subjects were studied twice according to a randomized, crossover protocol, involving one test with saline infusion and another with dichloroacetate infusion. Exercise load on a bicycle ergometer was increased progressively until exhaustion. Blood samples were drawn each minute throughout exercise and periodically throughout 120 min of recovery. Dichloroacetate significantly lowered the lactate concentration during exercise performed at less than 80% of the average maximal O2 consumption. The peak concentration of lactate at exhaustion was not affected by dichloroacetate treatment, but dichloroacetate did lower lactate concentration throughout recovery. These results suggest that a limitation in pyruvate dehydrogenase activity contributes to the increase in plasma lactate during submaximal exercise and recovery.
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Morita, Seiji, Takeshi Yamagiwa, Hiromichi Aoki, Keiji Sakurai i Sadaki Inokuchi. "Plasma lactate concentration as an indicator of plasma caffeine concentration in acute caffeine poisoning". Acute Medicine & Surgery 1, nr 3 (23.04.2014): 159–62. http://dx.doi.org/10.1002/ams2.28.
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Tonouchi, Mio, Hideo Hatta i Arend Bonen. "Muscle contraction increases lactate transport while reducing sarcolemmal MCT4, but not MCT1". American Journal of Physiology-Endocrinology and Metabolism 282, nr 5 (1.05.2002): E1062—E1069. http://dx.doi.org/10.1152/ajpendo.00358.2001.
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Rates of lactate uptake into giant sarcolemmal vesicles were determined in vesicles collected from rat muscles at rest and immediately after 10 min of intense muscle contraction. This contraction period reduced muscle glycogen rapidly by 37–82% in all muscles examined ( P < 0.05) except the soleus muscle (no change P > 0.05). At an external lactate concentration of 1 mM lactate, uptake into giant sarcolemmal vesicles was not altered ( P > 0.05), whereas at an external lactate concentration of 20 mM, the rate of lactate uptake was increased by 64% ( P < 0.05). Concomitantly, the plasma membrane content of monocarboxylate transporter (MCT)1 was reduced slightly (−10%, P < 0.05), and the plasma membrane content of MCT4 was reduced further (−25%, P < 0.05). In additional studies, the 10-min contraction period increased the plasma membrane GLUT4 ( P < 0.05) while again reducing MCT4 (−20%, P < 0.05) but not MCT1 ( P > 0.05). These studies have shown that intense muscle contraction can increase the initial rates of lactate uptake, but only when the external lactate concentrations are high (20 mM). We speculate that muscle contraction increases the intrinsic activity of the plasma membrane MCTs, because the increase in lactate uptake occurred while plasma membrane MCT4 was decreased and plasma membrane MCT1 was reduced only minimally, or not at all.
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Poso, A. R., T. Soveri, M. Alaviuhkola, L. Lindqvist, L. Alakuijala, P. H. Maenpaa i H. E. Oksanen. "Metabolic responses to exercise in the racehorse: changes in plasma alanine concentration". Journal of Applied Physiology 63, nr 6 (1.12.1987): 2195–200. http://dx.doi.org/10.1152/jappl.1987.63.6.2195.
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Previous studies in humans have shown that alanine is released from the skeletal muscle in proportion to the work load. We have measured plasma alanine and urea concentrations in well-trained Standardbred and Finnish-bred (cold-blooded) trotters after a graded-intensity exercise and during recovery to study metabolic responses to exercise in this animal model. As controls we measured blood lactate, pyruvate, and glucose concentrations as well as hematocrit values. Metabolic responses to exercise were closely reflected in all these parameters. Plasma alanine increased relatively more than plasma lactate at moderate-intensity exercise near anaerobic threshold. The linear correlation between the intensity of exercise and plasma alanine was similar to that observed earlier in humans. Interestingly, plasma alanine concentrations remained elevated long after the submaximal exercise, whereas the concentration of lactate, pyruvate, and glucose decreased more rapidly. No significant changes were found in plasma urea concentration under these conditions. The most significant differences in the metabolic responses to exercise of the two breeds studied were the higher lactate-to-pyruvate ratios achieved during the high-intensity exercise and the more sensitive increases of plasma alanine even during low-intensity exercise in the Finnish-bred horses. These differences probably reflect different compositions of muscle fiber types in the two breeds. The findings together indicate that plasma alanine is greatly increased in the racehorse during and after a high-intensity exercise and thus is an important vehicle in transporting ammonia and carbon skeletons of products of anaerobic glycolysis out of the muscle tissue.
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Jackson, Donald C., Carlos E. Crocker i Gordon R. Ultsch. "Bone and shell contribution to lactic acid buffering of submerged turtles Chrysemys picta bellii at 3°C". American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 278, nr 6 (1.06.2000): R1564—R1571. http://dx.doi.org/10.1152/ajpregu.2000.278.6.r1564.
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To evaluate shell and bone buffering of lactic acid during acidosis at 3°C, turtles were submerged in anoxic or aerated water and tested at intervals for blood acid-base status and plasma ions and for bone and shell percent water, percent ash, and concentrations of lactate, Ca2+, Mg2+, Pi, Na+, and K+. After 125 days, plasma lactate concentration rose from 1.6 ± 0.2 mM (mean ± SE) to 155.2 ± 10.8 mM in the anoxic group but only to 25.2 ± 6.4 mM in the aerated group. The acid-base state of the normoxic animals was stable after 25 days of submergence. Plasma calcium concentration ([Ca2+]) rose during anoxia from 3.2 ± 0.2 to 46.0 ± 0.6 mM and [Mg2+] from 2.7 ± 0.2 to 12.2 ± 0.6 mM. Both shell and bone accumulated lactate to concentrations of 135.6 ± 35.2 and 163.6 ± 5.1 mmol/kg wet wt, respectively, after 125 days anoxia. Shell and bone [Na+] both fell during anoxia but the fate of this Na+ is uncertain because plasma [Na+] also fell. No other shell ions changed significantly in concentration, although the concentrations of both bone calcium and bone potassium changed significantly. Control shell water (27.8 ± 0.6%) was less than bone water (33.6 ± 1.1%), but neither changed during submergence. Shell ash (44.7 ± 0.8%) remained unchanged, but bone ash (41.0 ± 1.0%) fell significantly. We conclude that bone, as well as shell, accumulate lactate when plasma lactate is elevated, and that both export sodium carbonate, as well as calcium and magnesium carbonates, to supplement ECF buffering.
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Nye, Carolyn J., Sarah E. Musulin, Rita M. Hanel i Christopher L. Mariani. "Evaluation of the Lactate Plus monitor for plasma lactate concentration measurement in dogs". Journal of Veterinary Emergency and Critical Care 27, nr 1 (14.12.2016): 66–70. http://dx.doi.org/10.1111/vec.12557.
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Taguchi, T., E. Yamashita, T. Mizutani, H. Nakajima, M. Yabuuchi, N. Asano i I. Miwa. "Hepatic glycogen breakdown is implicated in the maintenance of plasma mannose concentration". American Journal of Physiology-Endocrinology and Metabolism 288, nr 3 (marzec 2005): E534—E540. http://dx.doi.org/10.1152/ajpendo.00451.2004.
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d-Mannose is an essential monosaccharide constituent of glycoproteins and glycolipids. However, it is unknown how plasma mannose is supplied. The aim of this study was to explore the source of plasma mannose. Oral administration of glucose resulted in a significant decrease of plasma mannose concentration after 20 min in fasted normal rats. However, in fasted type 2 diabetes model rats, plasma mannose concentrations that were higher compared with normal rats did not change after the administration of glucose. When insulin was administered intravenously to fed rats, it took longer for plasma mannose concentrations to decrease significantly in diabetic rats than in normal rats (20 and 5 min, respectively). Intravenous administration of epinephrine to fed normal rats increased the plasma mannose concentration, but this effect was negated by fasting or by administration of a glycogen phosphorylase inhibitor. Epinephrine increased mannose output from the perfused liver of fed rats, but this effect was negated in the presence of a glucose-6-phosphatase inhibitor. Epinephrine also increased the hepatic levels of hexose 6-phosphates, including mannose 6-phosphate. When either lactate alone or lactate plus alanine were administered as gluconeogenic substrates to fasted rats, the concentration of plasma mannose did not increase. When lactate was used to perfuse the liver of fasted rats, a decrease, rather than an increase, in mannose output was observed. These findings indicate that hepatic glycogen is a source of plasma mannose.
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Yki-Järvinen, Hannele, Clifton Bogardus i James E. Foley. "Regulation of plasma lactate concentration in resting human subjects". Metabolism 39, nr 8 (sierpień 1990): 859–64. http://dx.doi.org/10.1016/0026-0495(90)90133-w.
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Jackson, D. "Lactate accumulation in the shell of the turtle Chrysemys picta bellii during anoxia at 3°C and 10°C". Journal of Experimental Biology 200, nr 17 (1.09.1997): 2295–300. http://dx.doi.org/10.1242/jeb.200.17.2295.
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Lactate concentrations were measured in the shell and plasma of the turtle Chrysemys picta bellii after 3 months of submergence anoxia at 3°C and during and after 9 days of submergence anoxia at 10°C. Liver and skeletal muscle lactate levels were also measured in control and anoxic animals at each temperature. At 3°C, mean shell lactate concentration (N=4) reached 133mmolkg-1shellmass and plasma lactate levels were 144mmoll-1; at 10°C, shell and plasma lactate concentrations (N=5) rose in parallel during anoxic exposure, to 70.8mmolkg-1shellmass and 78.9mmoll-1, respectively, and returned in parallel to control levels during 9 days of recovery. At the end of the anoxic periods, an estimated 44% of the total body lactate resided in the shell at 3°C and 43% at 10°C, and indirect evidence suggests that the shell buffered these same fractions of the acid load. Because of the high lactate concentration per kilogram of shell water (416mmolkg-1 at 3°C; 221mmolkg-1 at 10°C) and the known formation of calcium lactate complexes, it is postulated that most of the lactate existed in the shell in combined form. I conclude that sequestration of lactate within the shell represents a potentially major adaptation to anoxic acidosis for this animal and, together with the previously described release of shell carbonates, may account for up to two-thirds of the total lactic acid buffering in this animal.
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Weber, J. M., W. S. Parkhouse, G. P. Dobson, J. C. Harman, D. H. Snow i P. W. Hochachka. "Lactate kinetics in exercising Thoroughbred horses: regulation of turnover rate in plasma". American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 253, nr 6 (1.12.1987): R896—R903. http://dx.doi.org/10.1152/ajpregu.1987.253.6.r896.
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Plasma lactate turnover rate of Thoroughbred racehorses was measured by bolus injection of [U-14C]lactate at rest and two levels of submaximal treadmill exercise (3-4 m/s trot, 6% incline, and 6.5 m/s horizontal canter). Our goals were 1) to determine the relative effects of changes in cardiac output and in plasma lactate concentration on turnover rate [using cardiac output data from Weber et al. (28)] and 2) to assess the importance of lactate as a metabolic fuel in a trained animal athlete. Lactate turnover rates were 9.3 mumol.min-1.kg-1 (rest), 75.9 mumol.min-1.kg-1 at the beginning of the trot protocol [45% maximum O2 uptake (VO2max)], 50.3 mumol.min-1.kg-1 later in the same protocol (50% VO2max), and 66.1 mumol.min-1.kg-1 during the canter protocol (55% VO2max). Both changes in cardiac output and in plasma lactate concentration had a significant effect on turnover rate. Variation in plasma lactate fluxes of Thoroughbreds during exercise follows the standard mammalian pattern, but this substrate only plays a minor role as an oxidizable fuel in horses. The oxidation of plasma lactate accounts for less than 5% of metabolic rate (VO2) during submaximal work. Adjustments in cardiac output and in metabolite concentration represent, respectively, the coarse and fine controls for the regulation of plasma metabolite turnover rate.
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MacLean, Dave A., Jens Bangsbo i Bengt Saltin. "Muscle interstitial glucose and lactate levels during dynamic exercise in humans determined by microdialysis". Journal of Applied Physiology 87, nr 4 (1.10.1999): 1483–90. http://dx.doi.org/10.1152/jappl.1999.87.4.1483.
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The purpose of the present study was to use the microdialysis technique to determine skeletal muscle interstitial glucose and lactate concentrations during dynamic incremental exercise in humans. Microdialysis probes were inserted into the vastus lateralis muscle, and subjects performed knee extensor exercise at workloads of 10, 20, 30, 40, and 50 W. The in vivo probe recoveries determined at rest by the internal reference method for glucose and lactate were 28.7 ± 2.5 and 32.0 ± 2.7%, respectively. As exercise intensity increased, probe recovery also increased, and at the highest workload probe recovery for glucose (61.0 ± 3.9%) and lactate (66.3 ± 3.6%) had more than doubled. At rest the interstitial glucose concentration (3.5 ± 0.2 mM) was lower than both the arterial (5.6 ± 0.2 mM) and venous (5.3 ± 0.3 mM) plasma water glucose levels. The interstitial glucose levels remained lower ( P < 0.05) than the arterial and venous plasma water glucose concentrations during exercise at all intensities and at 10, 20, 30, and 50 W, respectively. At rest the interstitial lactate concentration (2.5 ± 0.2 mM) was higher ( P < 0.05) than both the arterial (0.9 ± 0.2 mM) and venous (1.1 ± 0.2 mM) plasma water lactate levels. This relationship was maintained ( P < 0.05) during exercise at workloads of 10, 20, and 30 W. These data suggest that interstitial glucose delivery at rest is flow limited and that during exercise changes in the interstitial concentrations of glucose and lactate mirror the changes observed in the venous plasma water compartments. Furthermore, skeletal muscle contraction results in an increase in the diffusion coefficient of glucose and lactate within the interstitial space as reflected by an elevation in probe recovery during exercise.
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Weber, Jean-Michel, Wade S. Parkhouse, Geoffrey P. Dobson, Joyce C. Harman, David H. Snow i Peter W. Hochachka. "Onset of submaximal exercise in thoroughbred horses". Canadian Journal of Zoology 65, nr 10 (1.10.1987): 2513–18. http://dx.doi.org/10.1139/z87-379.
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Plasma lactate concentration, hematocrit, and heart rate were measured during a 40-min trot (3–4 m/s, 6% incline) and a 15-min canter (6.5 m/s, 0% incline) in catheterized thoroughbred horses running on a treadmill to characterize the transient changes in plasma lactate concentration during the onset of exercise, and to determine if and when a steady state was established. The intensity of exercise had an effect on the pattern of changes observed for the three variables investigated. Mean hematocrit rose from 38.5% at rest to 52.0% after a 4-min walk (1.6 m/s) and to 57.7% after 3 min of subsequent trotting (4 m/s). The highest mean value of 58.7% was reached after 3 min of cantering. A slow but significant decrease in hematocrit was measured between the time maximum levels were attained for each work intensity and the end of exercise. During the onset of submaximal work, plasma lactate concentration, hematocrit, and heart rate all reached a maximum simultaneously. The rapid cardiovascular response of thoroughbreds (strong hematocrit increase and heart-rate overshoot) did not prevent them from temporarily relying on anaerobic metabolism, as shown by a marked lactate overshoot before a steady state was established. The observed changes in lactate concentration are explained by a model predicting lactate fluxes to and from the plasma compartment during the transition from the resting steady state to the exercise steady state. Biopsies of the middle gluteal muscle were taken before and after the canter protocol to measure the metabolic intermediates of the glycogenolytic pathway. The resting and postexercise concentrations of these intermediates were not different except for a 30% reduction in glycogen. Aerobic glycogenolysis was the main pathway for energy metabolism in the middle gluteus and, as in plasma, a metabolic steady state was established in this muscle.
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Feriani, Mariano, Claudio Ronco i Giuseppe La Greca. "Acid-Base Balance with Different Capd Solutions". Peritoneal Dialysis International: Journal of the International Society for Peritoneal Dialysis 16, nr 1_suppl (styczeń 1996): 126–29. http://dx.doi.org/10.1177/089686089601601s23.
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Our objective is to investigate transperitoneal buffer fluxes with solution containing lactate and bicarbonate, and to compare the final effect on body base balance of the two solutions. One hundred and four exchanges, using different dwell times, were performed in 52 stable continuous ambulatory peritoneal dialysis (CAPD) patients. Dialysate effluent lactate and bicarbonate and volumes were measured. Net dialytic base gain was calculated. Patients’ acid-base status and plasma lactate were determined. In lactate-buffered CAPD solution, lactate concentration in dialysate effluent inversely correlated with length of dwell time, but did not correlate with plasma lactate concentration and net ultrafiltration. Bicarbonate concentration in dialysate effluent correlated with plasma bicarbonate and dwell time but not with ultrafiltration. The arithmetic sum of the lactate gain and bicarbonate loss yielded the net dialytic base gain. Ultrafiltration was the most important factor affecting net dialytic base gain. A previous study demonstrated that in patients using a bicarbonate-buffered solution the net bicarbonate gain is a function of dwell time, ultrafiltration, and plasma bicarbonate. By combining the predicted data of the dialytic base gain with the calculated metabolic acid production, an approximate body base balance could be obtained with both lactate and bicarbonate-buffered CAPD solutions. The body base balance in CAPD patients is self-regulated by the feedback between plasma bicarbonate concentration and dialytic base gain. The level of plasma bicarbonate is determined by the dialytic base gain and the metabolic acid production. This can explain the large interpatient variability in acid-base correction. Bicarbonate-buffered CAPD solution is equal to lactate solution in correcting acid-base disorders of CAPD patients.
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Fattor, Jill A., Benjamin F. Miller, Kevin A. Jacobs i George A. Brooks. "Catecholamine response is attenuated during moderate-intensity exercise in response to the “lactate clamp”". American Journal of Physiology-Endocrinology and Metabolism 288, nr 1 (styczeń 2005): E143—E147. http://dx.doi.org/10.1152/ajpendo.00117.2004.
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Catecholamine release is known to be regulated by feedforward and feedback mechanisms. Norepinephrine (NE) and epinephrine (Epi) concentrations rise in response to stresses, such as exercise, that challenge blood glucose homeostasis. The purpose of this study was to assess the hypothesis that the lactate anion is involved in feedback control of catecholamine concentration. Six healthy active men (26 ± 2 yr, 82 ± 2 kg, 50.7 ± 2.1 ml·kg−1·min−1) were studied on five occasions after an overnight fast. Plasma concentrations of NE and Epi were determined during 90 min of rest and 90 min of exercise at 55% of peak O2 consumption (V̇o2 peak) two times with exogenous lactate infusion (lactate clamp, LC) and two times without LC (CON). The blood lactate profile (∼4 mM) of a preliminary trial at 65% V̇o2 peak (65%) was matched during the subsequent LC trials. In resting men, plasma NE concentration was not different between trials, but during exercise all conditions were different with 65% > CON > LC (65%: 2,115 ± 166 pg/ml, CON: 1,573 ± 153 pg/ml, LC: 930 ± 174 pg/ml, P < 0.05). Plasma Epi concentrations at rest were different between conditions, with LC less than 65% and CON (65%: 68 ± 9 pg/ml, CON: 59 ± 7 pg/ml, LC: 38 ± 10 pg/ml, P < 0.05). During exercise, Epi concentration showed the same trend (65%: 262 ± 37 pg/ml, CON: 190 ± 34 pg/ml, LC: 113.2 ± 23 pg/ml, P < 0.05). In conclusion, lactate attenuates the catecholamine response during moderate-intensity exercise, likely by feedback inhibition.
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Scheingraber, Stefan, Markus Rehm, Christiane Sehmisch i Udilo Finsterer. "Rapid Saline Infusion Produces Hyperchloremic Acidosis in Patients Undergoing Gynecologic Surgery". Anesthesiology 90, nr 5 (1.05.1999): 1265–70. http://dx.doi.org/10.1097/00000542-199905000-00007.
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Background Changes in acid-base balance caused by infusion of a 0.9% saline solution during anesthesia and surgery are poorly characterized. Therefore, the authors evaluated these phenomena in a dose-response study. Methods Two groups of 12 patients each who were undergoing major intraabdominal gynecologic surgery were assigned randomly to receive 0.9% saline or lactated Ringer's solution in a dosage of 30 ml x kg(-1) x h(-1). The pH, arterial carbon dioxide tension, and serum concentrations of sodium, potassium, chloride, lactate, and total protein were measured in 30-min intervals. The serum bicarbonate concentration was calculated using the Henderson-Hasselbalch equation and also using the Stewart approach from the strong ion difference and the amount of weak plasma acid. The strong ion difference was calculated as serum sodium + serum potassium - serum chloride - serum lactate. The amount of weak plasma acid was calculated as the serum total protein concentration in g/dl x 2.43. Results Infusion of 0.9% saline, but not lactated Ringer's solution, caused a metabolic acidosis with hyperchloremia and a concomitant decrease in the strong ion difference. Calculating the serum bicarbonate concentration using the Henderson-Hasselbalch equation or the Stewart approach produced equivalent results. Conclusions Infusion of approximately 30 ml x kg(-1) x h(-1) saline during anesthesia and surgery inevitably leads to metabolic acidosis, which is not observed after administration of lactated Ringer's solution. The acidosis is associated with hyperchloremia.
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Fonseca, L. A., F. M. Girardi, C. S. Coelho, G. Barioni, V. B. Rangel i R. C. Gonçalves. "Influence of chromium supplementation on energy metabolism in horses used in policing activity". Arquivo Brasileiro de Medicina Veterinária e Zootecnia 63, nr 5 (październik 2011): 1175–80. http://dx.doi.org/10.1590/s0102-09352011000500019.
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The influence of chromium supplementation on some blood variables in 11 adult stallions used for policing activities was evaluated. Each animal was treated with 11mg of chromium/400kg body weight, orally, for a period of 30 days. On days 0 (before) and 30 (after) the animals were evaluated and blood samples were obtained before and after exercise. Plasma glucose and lactate and serum cortisol and insulin were analyzed in each of these moments. On day 0, plasma glucose concentrations were 68.4±5.6mg/dL and 78.7±6.5mg/dL; plasma lactate concentrations were 6.2±0.6mg/dL and 13.1±7.6mg/dL; serum cortisol values were 48.5±7.9ng/mL and 42.6±19.7ng/mL; and serum insulin values were 3.0±6.4µUI/mL and 1.9±1.7µUI/mL, respectively, before and after exercise. On day 30, plasma glucose concentrations were 73.3±5.7mg/dL and 78.4±6.7mg/dL; plasma lactate concentrations were 7.3±0.9mg/dL and 7.6±1.2mg/dL; serum cortisol values were 62.9±21.8ng/mL and 40.3±17.0ng/mL; and serum insulin values were 1.4±1.3µUI/mL and 1.7±1.4µUI/mL, respectively, before and after exercise. As an effect of the exercise, a decrease was shown in the concentration of serum insulin and an increase in plasma lactate and glucose. Chromium supplementation resulted in a reduction of lactate values after physical activity, possibly indicating that chromium contributed to a better utilization of plasma glucose and to a better adaptation of animals to physical activity.
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Stannard, Stephen R., Martin W. Thompson i Janette C. Brand Miller. "The Effect of Glycemic Index on Plasma Glucose and Lactate Levels during Incremental Exercise". International Journal of Sport Nutrition and Exercise Metabolism 10, nr 1 (marzec 2000): 51–61. http://dx.doi.org/10.1123/ijsnem.10.1.51.
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Consumption of low glycemic index (GI) foods before submaximal endurance exercise may be beneficial to performance. To test whether this may also be true for high intensity exercise. 10 trained cyclists began an incremental exercise test to exhaustion 65 min after consuming equal carbohydrate portions of glucose (HGI), pasta (LGI), and a noncarbohydrate control (PL). Time to fatigue did not differ significantly (p = 0.05) between treatments. Plasma glucose concentration was significantly lower after LGI vs. HGI from 15 to 45 min of rest postprandial. During exercise, plasma glucose concentration was significantly lower after HGI vs. LGI from 200 W until exhaustion. Plasma lactate concentration following HGI was significantly higher than PL from 30 min of rest postprandial through to the end of the 200-W workload. Plasma lactate concentration following LGI was significantly lower than after HGI from 45 min of rest postprandial through to the end of the 100-W workload. At higher exercise intensities, there was no significant difference in plasma lactate levels between treatments. These findings suggest that a high GI carbohydrate meal (1 g/kg body wt) 65 min prior to exercise decreases plasma glucose and increases plasma lactate levels compared to a low GI meal, but not enough to be detrimental to incremental exercise performance.
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Bocking, A. D., L. J. Carmichael, S. Abdollah, K. R. Sinervo, G. N. Smith i J. F. Brien. "Effect of ethanol on immature ovine fetal breathing movements, fetal prostaglandin E2, and myometrial activity". American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 266, nr 4 (1.04.1994): R1297—R1301. http://dx.doi.org/10.1152/ajpregu.1994.266.4.r1297.
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In the mature ovine fetus, ethanol decreases fetal breathing movements (FBM), which is temporally related to increased prostaglandin E2 (PGE2) concentration, decreases blood glucose concentration, increases blood lactate concentration, and decreases uterine electromyographic (EMG) activity. The objective of this study was to determine the effects of ethanol on these variables in the immature fetal sheep. Experiments were conducted in pregnant ewes at 85-94 days of gestation (full term 147 days) that received a 1-h maternal infusion of 1 g ethanol/kg maternal body wt (n = 9) or an equivalent volume of saline (n = 5). The maximal maternal and fetal blood ethanol concentrations for the ethanol regimen were 1.305 +/- 0.165 and 1.458 +/- 0.137 mg/ml, respectively. Maternal infusion of ethanol (or saline) did not change the incidence of FBM, fetal plasma PGE2 concentration, heart rate, blood pressure, blood gases and pH, or uterine EMG activity. Ethanol decreased (P < 0.05) fetal blood glucose concentration from 1.18 +/- 0.10 to 0.87 +/- 0.07 and 0.89 +/- 0.09 mM at 1 and 3 h, respectively, but did not alter blood lactate concentration compared with saline infusion. These data support the hypothesis that the effects of ethanol on FBM, fetal plasma PGE2 and blood lactate concentrations, and uterine EMG activity are gestational age dependent.
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Moritz, A., M. Kramer, N. Bauer i J. Verschoof. "Hemostatic variables, plasma lactate concentration, and inflammatory biomarkers in dogs with gastric dilatation-volvulus". Tierärztliche Praxis Ausgabe K: Kleintiere / Heimtiere 43, nr 06 (2015): 389–98. http://dx.doi.org/10.15654/tpk-150284.
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Summary Objective: Prospective characterization of hemostastatic variables, plasma lactate concentration, and inflammatory biomarkers in dogs with gastric dilatation-volvulus (GDV). Material and methods: Coagulation variables (platelets, prothrombin time [PT], activated partial thromboplastin time [aPTT], fibrinogen, antithrombin [AT], protein C [PC], protein S [PS], D-dimers), plasma lactate concentration and inflammatory biomarkers (C-reactive protein, white blood cell [WBC] count, lymphocyte and neutrophil numbers) were assessed in 20 dogs with GDV presented between 2011 and 2012. Blood was taken preoperatively and at days 1 and 3 postoperatively. The prognostic value of these variables before and after surgery was evaluated as well as the behavior of variables during the study. Results: Overall, 7/20 (35%) dogs did not survive; two dogs (29%) were euthanized during surgery due to severe gastric necrosis and 5 (71%) dogs after surgery due to sepsis and disseminated intravascular coagulopathy. Prior to surgery, median plasma lactate concentration was significantly (p = 0.01) lower in survivors (6.2 mmol/l, range 1.9–9.7 mmol/l) when compared to non-survivors (11.8 mmol/l, range 7.5–16.2 mmol/l). In dogs dying after surgery, significantly higher plasma lactate concentration, coagulation times and D-dimer concentration were present as well as lower fibrinogen concentration and activity of PC and AT compared to survivors. At discharge, activity of AT, PC and PS were markedly below the reference interval in 6/13 (46%), 11/13 (85%), and 8/13 (62%) dogs, respectively. Clinical relevance: Only lactate plasma concentration was of preoperative prognostic value. After surgery, severe abnormalities of coagulation variables, especially the endogenous anticoagulants were present in most of the dogs. The severity of the abnormalities was associated with survival.
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Miller, Benjamin F., Michael I. Lindinger, Jill A. Fattor, Kevin A. Jacobs, Paul J. LeBlanc, MyLinh Duong, George J. F. Heigenhauser i George A. Brooks. "Hematological and acid-base changes in men during prolonged exercise with and without sodium-lactate infusion". Journal of Applied Physiology 98, nr 3 (marzec 2005): 856–65. http://dx.doi.org/10.1152/japplphysiol.00753.2004.
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An emerging technique used for the study of metabolic regulation is the elevation of lactate concentration with a sodium-lactate infusion, the lactate clamp (LC). However, hematological and acid-base properties affected by the infusion of hypertonic solutions containing the osmotically active strong ions sodium (Na+) and lactate (Lac−) are a concern for clinical and research applications of LC. In the present study, we characterized the hematological and plasma acid-base changes during rest and prolonged, light- to moderate-intensity (55% V̇o2 peak) exercise with and without LC. During the control (Con) trial, subjects were administered an isotonic, isovolumetric saline infusion. During LC, plasma lactate concentration ([Lac−]) was elevated to 4 meq/l during rest and to 4–7 meq/l during exercise. During LC at rest, there were rapid and transient changes in plasma, erythrocyte, and blood volumes. LC resulted in decreased plasma [H+] (from 39.6 to 29.6 neq/l) at the end of exercise while plasma [HCO3−] increased from 26 to 32.9 meq/l. Increased plasma strong ion difference [SID], due to increased [Na+], was the primary contributor to decreased [H+] and increased [HCO3−]. A decrease in plasma total weak acid concentration also contributed to these changes, whereas Pco2 contributed little. The infusion of hypertonic LC caused only minor volume, acid-base, and CO2 storage responses. We conclude that an LC infusion is appropriate for studies of metabolic regulation.
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Gladden, L. B., R. E. Crawford i M. J. Webster. "Effect of lactate concentration and metabolic rate on net lactate uptake by canine skeletal muscle". American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 266, nr 4 (1.04.1994): R1095—R1101. http://dx.doi.org/10.1152/ajpregu.1994.266.4.r1095.
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This study addressed two questions: 1) Does net lactate uptake (L) by muscle approach a saturation limit with increasing blood lactate concentration ([La])? 2) Is the muscle net L response to increasing blood [La] affected by metabolic rate (VO2)? The gastrocnemius plantaris muscle group (GP) was isolated in situ in 20 anesthetized dogs. In three series of experiments, a lactate-lactic acid solution was infused into the arterial inflow of the GP to produce five different plasma [La] values: approximately 3, 9, 16, 22, and 30 mM, each of them maintained for 30 min. In one series, the GP remained at rest, whereas in the second series it contracted at 1 Hz and in the third series at 4 Hz. VO2 averaged approximately 3, 43, and 100 ml.kg-1.min-1 at rest and at 1 and 4 Hz, respectively. Within each of the three metabolic rates, increasing plasma [La] resulted in an increase in net L, which was well described (R > 0.98) by exponential equations. These equations predicted net L asymptotic values of 0.80, 0.72, and 1.09 mmol.kg-1.min-1 for rest and for 1 and 4 Hz, respectively. The corresponding plasma [La]s for half-maximal net L from the exponential equations were 16, 10, and 12 mM. Glucose uptake, pyruvate uptake/output, and alanine output by the muscles were not affected by the increasing [La] (and concomitant increases in net L) at any of the metabolic rates. Neither net glycogen synthesis nor depletion was changed by increasing [La].(ABSTRACT TRUNCATED AT 250 WORDS)
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Cecca, M., D. MacDougall, N. Tsunoda i F. O??Hagan. "THE VENTILATORY THRESHOLD IS NOT RELATED TO PLASMA LACTATE CONCENTRATION". Medicine & Science in Sports & Exercise 18, supplement (kwiecień 1986): S85. http://dx.doi.org/10.1249/00005768-198604001-00421.
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Hildebrand, A., W. Lormes, J. Emmert, Y. Liu, M. Lehmann i J. M. Steinacker. "Lactate Concentration in Plasma and Red Blood CellsDuring Incremental Exercise". International Journal of Sports Medicine 21, nr 7 (październik 2000): 463–68. http://dx.doi.org/10.1055/s-2000-7412.
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Washburn, B. S., J. S. Krantz, E. H. Avery i R. A. Freedland. "Effects of estrogen on gluconeogenesis and related parameters in male rainbow trout". American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 264, nr 4 (1.04.1993): R720—R725. http://dx.doi.org/10.1152/ajpregu.1993.264.4.r720.
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To investigate the effects of estrogen, the hormone responsible for vitellogenesis, on gluconeogenesis, male rainbow trout were implanted with 17 beta-estradiol or given a sham procedure. Plasma glucose concentration in estrogenized fish was 50% of the control fish (6.4 mM). Glucose synthesis from physiological concentrations of alanine was 0.08 mumol.g cells-1 x h-1 compared with 0.20 mumol.g cells-1 x h-1 in control fish; synthesis from physiological concentrations of lactate was reduced by over 50% (0.88 vs. 0.36 mumol.g cells-1 x h-1) in implanted fish. Gluconeogenesis from 5 mM lactate was also significantly depressed in implanted fish. Oxidation of alanine, serine, and lactate was not significantly affected by estrogen implantation. The maximum clearance velocity of a key enzyme negatively regulating gluconeogenesis, pyruvate kinase, was 3.03 mumol.g cells-1 x h-1 in estrogen (E2) implanted fish compared with 7.83 mumol.g cells-1 x h-1 in control fish. No significant differences in plasma insulin or glucagon were found in the two groups. We conclude that estrogen depresses gluconeogenesis and that this reduction contributes to the lower plasma glucose concentration seen in vitellogenic trout.
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Kitaoka, Y., K. Mukai, K. Takahashi, H. Ohmura i H. Hatta. "Effect of lactate administration on exercise-induced PGC-1α mRNA expression in Thoroughbreds". Comparative Exercise Physiology 16, nr 4 (1.07.2020): 253–58. http://dx.doi.org/10.3920/cep200009.
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The aim of this study was to examine the effects of lactate administration on the mRNA response of peroxisome proliferator-activated receptor gamma coactivator 1-alpha (PGC-1α) to acute exercise in Thoroughbred skeletal muscle. Five Thoroughbred horses performed treadmill running at 90% of maximal oxygen consumption for 2 min on two separate occasions, either after the administration of two litres of a sodium lactate solution (LAC; 500 mmol/l sodium lactate in 0.9% NaCl) or a saline solution as a control (CON; 0.9% NaCl). Lactate administration significantly elevated the peak plasma lactate concentration during exercise (16.0±2.8 mmol/l in LAC vs 10.8±2.2 mmol/l in CON). The increase in PGC-1α mRNA expression after 4 h of recovery from exercise was similar between treatments. However, there was positive correlation between exercise-induced PGC-1α mRNA response at 4 h after exercise and peak plasma lactate concentration during exercise. These results suggest that the exercise intensity-dependent adaptation of PGC-1α may be attributed, at least in part, to an increased lactate concentration.
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Stämpfli, Henry, Michael Taylor, Carl McNicoll, Ady Y. Gancz i Peter D. Constable. "Experimental determination of net protein charge, [A]tot, and Ka of nonvolatile buffers in bird plasma". Journal of Applied Physiology 100, nr 6 (czerwiec 2006): 1831–36. http://dx.doi.org/10.1152/japplphysiol.01367.2005.
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The quantitative mechanistic acid-base approach to clinical assessment of acid-base status requires species-specific values for [A]tot (the total concentration of nonvolatile buffers in plasma) and Ka (the effective dissociation constant for weak acids in plasma). The aim of this study was to determine [A]tot and Ka values for plasma in domestic pigeons. Plasma from 12 healthy commercial domestic pigeons was tonometered with 20% CO2 at 37°C. Plasma pH, Pco2, and plasma concentrations of strong cations (Na, K, Ca), strong anions (Cl, l-lactate), and nonvolatile buffer ions (total protein, albumin, phosphate) were measured over a pH range of 6.8–7.7. Strong ion difference (SID) (SID5 = Na + K + Ca − Cl − lactate) was used to calculate [A]tot and Ka from the measured pH and Pco2 and SID5. Mean (±SD) values for bird plasma were as follows: [A]tot = 7.76 ± 2.15 mmol/l (equivalent to 0.32 mmol/g of total protein, 0.51 mmol/g of albumin, 0.23 mmol/g of total solids); Ka = 2.15 ± 1.15 × 10−7; and p Ka = 6.67. The net protein charge at normal pH (7.43) was estimated to be 6 meq/l; this value indicates that pigeon plasma has a much lower anion gap value than mammals after adjusting for high mean l-lactate concentrations induced by restraint during blood sampling. This finding indicates that plasma proteins in pigeons have a much lower net anion charge than mammalian plasma protein. An incidental finding was that total protein concentration measured by a multianalyzer system was consistently lower than the value for total solids measured by refractometer.
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Soloveva, A. G., i S. P. Peretyagin. "The effect of subchronic inhalations of nitric oxide on metabolic processes in blood of experimental animals". Biomeditsinskaya Khimiya 62, nr 2 (2016): 212–14. http://dx.doi.org/10.18097/pbmc20166202212.
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Metabolic processes were investigated in plasma and erythrocytes of Wistar rats exposed to daily 10-min sessions of NO inhalation for 30 days. These included determination of glucose and lactate, catalase activity, and activities of aldehyde dehydrogenase (ALDH), lactate dehydrogenase (LDH), and catalase. NO inhalation in a concentration of 20 ppm, 50 ppm and 100 ppm caused an increase in glucose and lactate. Inhalation of 100 ppm NO also increased catalase activity. Inhalation of all NO concentrations resulted in a decrease of ALDH activity, while the decrease in LDH activity was observed at NO concentrations of 50-100 ppm
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PAVLIDOU (Κ. ΠΑΥΛΙΔΟΥ), K., I. SAVVAS (Ι. ΣΑΒΒΑΣ) i G. KAZAKOS (Γ. ΚΑΖΑΚΟΣ). "Lactate in intensive care unit". Journal of the Hellenic Veterinary Medical Society 60, nr 4 (21.11.2017): 553. http://dx.doi.org/10.12681/jhvms.14942.
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Lactate is produced in cells under anaerobic conditions. Hyperlactatemia is the increase of the plasma lactateconcentration and lactic acidosis is the elevation in lactate concentration with a decrease in arterial pH. Hyperlactatemia and lactic acidosis are common in shock, but may also occur in many other clinical syndromes. Clinical studies in humans have reported that lactate concentration may contribute to the diagnosis of diseases in an intensive care unit and the estimation of the prognosis. In veterinary literature, clinical trials on lactate concentration in critical patients are rare, however, there are reports indicating its potential significance. Moreover, the severity of disease is linked to high lactate concentrations in the arterial blood, which is considered to be a negative prognostic index, at least in dogs. Lactate is formed in skeletal muscles, brain, heart, skin, intestinal tract, red and white blood cells. In the liver and kidneys it is metabolized up to 50%. In most human cases in intensive care units, hyperlactatemia and lactic acidosis are the result of hypoxia and tissue hypoperfusion. These patients are in a great risk of developing multi-organ failure and they present with high mortality rates. The persistent systemic acidosis affects myocardial contractility, reduces cardiac output and organ perfusion and leads to severe hypoxia. The causes of hyperlactatemia are: high glycolytic flux (alkalosis, release of catecholamine), high production of pyruvate acid and increased metabolic state conditions. Lactic acidosis may be of type A or type B. Lactate concentration can be measured either in whole blood or plasma by two methods: enzymatic chromatography and enzymatic amperometry. The lactate measurement in intensive care units is important, as it can be used to assess organ hypoperfusion and hypoxia, effectiveness of treatment and prognosis of various pathological conditions, such as septic peritonitis, gastric volvulus, pyometra and babesiosis. The treatment of lactic acidosis depends on the severity and management of the underlying disease. The goal of treatment is adequate tissue perfusion and oxygenation, which is achieved by ventilation and fluid therapy. The microbial infections are treated with antibiotics. The use of bicarbonate is still controversial.
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Laughlin, M. R., J. Taylor, A. S. Chesnick, M. DeGroot i R. S. Balaban. "Pyruvate and lactate metabolism in the in vivo dog heart". American Journal of Physiology-Heart and Circulatory Physiology 264, nr 6 (1.06.1993): H2068—H2079. http://dx.doi.org/10.1152/ajpheart.1993.264.6.h2068.
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Pyruvate increases the phosphorylation potential in perfused heart to a greater extent than the closely correlated substrate L-lactate. Therefore, metabolism of these compounds was studied in the myocardium of intact dogs. Phosphocreatine/ATP was increased 23% at 5.3 mM plasma pyruvate but was not significantly increased by lactate except at the highest concentration (17.5 mM in blood). Calculated [ADP] fell during pyruvate infusion from 51.5 +/- 2.0 to 38.6 +/- 3.3 microM but did not change significantly during lactate infusion. Intracellular free [Mg2+] fell from 705 +/- 53 to 498 +/- 30 microM at the highest pyruvate infusion and from 692 +/- 112 to 417 +/- 19 microM with lactate infusion. Extraction of both substrates was linear at low concentrations, reaching 0.56 mumol lactate.min-1.g wet wt-1 at 17.5 mM blood lactate and 0.58 mumol pyruvate.min-1.g wet wt-1 at 5.3 mM plasma pyruvate. Therefore, lactate uptake was almost five times lower than pyruvate uptake at similar concentrations. Elevated pyruvate (> 3 mM) resulted in almost complete inhibition of net lactate uptake. Infused [3-13C]lactate or -pyruvate gave rise to labeled glutamate and alanine in vivo, but labeled lactate was not visible when [3–13C]pyruvate was the substrate. The 13C enrichment of myocardial lactate was similar to alanine and acetyl CoA with infused [3–13C]lactate but was only one-half that of alanine and acetyl CoA when [3–13C]-pyruvate was the substrate, indicating a possible inhibition of lactate dehydrogenase.
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Duan, Yan, Mengyao Li, Ming Sun, Aiyong Wang, Yu Chai, Jing Dong, Fudi Chen, Zhe Yu i Xiumei Zhang. "Effects of Salinity and Dissolved Oxygen Concentration on the Tail-Flip Speed and Physiologic Response of Whiteleg Shrimp, Litopenaeus vannamei". Sustainability 14, nr 22 (20.11.2022): 15413. http://dx.doi.org/10.3390/su142215413.
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The swimming ability of shrimp is important for their survival and growth, which directly affects their avoidance of enemies and uncomfortable environment, search and capture of food, reproductive behavior, and distribution. The knowledge concerning the swimming ability of shrimp can be widely used in the conservation of fishery resources, improving capture efficiency and stock enhancement. As one of the edible marine organisms, Litopenaeus vannamei is a traditional fishery resource and an important economic aquaculture species in China. Dissolved oxygen (DO) concentration and salinity are considered to play crucial roles in the swimming ability of L. vannamei. The tail-flip speed (Stf) of whiteleg shrimp L. vannamei (79.90 ± 0.41 mm, 5.76 ± 0.10 g) that were exposed to various salinities (20‰, 25‰, 30‰, 35‰, and 40‰) and DO concentrations (1.9, 3.8, 6.8, and 13.6 mg/L) was determined under laboratory conditions. Metabolite concentrations in the hemolymph, hepatopancreas, and abdominal muscles were measured before and after tail-flip fatigue to evaluate the physiologic effects of fatigue in L. vannamei. The results showed that salinity and DO significantly affected the Stf of L. vannamei. The Stf increased and subsequently decreased with the increase in salinity from 20‰ to 40‰. The relationship between Stf and salinity (s, ‰) can be expressed by the quadratic model as Stf = −0.2386s2 + 15.528s − 145.12, R2 = 0.9693. The optimum salinity and corresponding maximum Stf were 32.54‰ and 107.52 cm/s, respectively. The Stf increased as the DO concentration increased from 1.9 mg/L to 13.6 mg/L. The relationship between Stf and DO (mg/L) can be expressed by the power model as Stf = 75.621 DO0.1753, R2 = 0.9981. The different salinities and DO concentrations directly affected the physiology of the shrimp, inducing changes in hepatopancreas total protein, plasma total protein, abdominal muscle lactate, plasma lactate, plasma glucose, hepatopancreas glycogen, and abdominal muscle glycogen concentration. Fatigue from tail-flip led to severe loss of hepatopancreas glycogen under 20‰ salinity and plasma glucose under 25‰, 30‰, and 35‰ salinity. The triglyceride and lactate in the plasma concentration increased significantly in a range of salinities. In the DO concentration experiment, fatigue from tail-flip led to a severe loss of plasma glucose under 1.9 mg/L and 3.8 mg/L DO concentrations. The plasma lactate concentration increased significantly in all DO groups. The results suggested that the inappropriate salinity and DO significantly limited the tail-flip speed of shrimp, which was due to the accumulation of metabolites. The proper salinity and DO accelerated the elimination of metabolites, reduced the energy consumption of shrimp, and thus, improved the exercise ability of shrimp. This conclusion is of particular value in evaluating the swimming ability of shrimp and understanding its ecological processes to improve capture and rearing techniques.
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Petibois, Cyril, Georges Cazorla, André Cassaigne i Gérard Déléris. "Plasma Protein Contents Determined by Fourier-Transform Infrared Spectrometry". Clinical Chemistry 47, nr 4 (1.04.2001): 730–38. http://dx.doi.org/10.1093/clinchem/47.4.730.
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Abstract Background: Fourier-transform infrared (FT-IR) spectrometry has been used to measure small molecules in plasma. We wished to extend this use to measurement of plasma proteins. Methods: We analyzed plasma proteins, glucose, lactate, and urea in 49 blood samples from 35 healthy subjects and 14 patients. For determining the concentration of each biomolecule, the method used the following steps: (a) The biomolecule was sought for which the correlation between spectral range areas of plasma FT-IR spectra and concentrations determined by comparison method was greatest. (b) The IR absorption of the biomolecule at the most characteristic spectral range was calculated by analyzing pure samples of known concentrations. (c) The plasma concentration of the biomolecule was determined using the FT-IR absorption of the pure compound and the integration value obtained for the plasma FT-IR spectra. (d) The spectral contribution of the biomolecule was subtracted from the plasma FT-IR spectra, and the resulting spectra were saved for further analyses. (e) The same method was then applied to determining the concentrations of other biomolecules by sequentially comparing the resulting FT-IR spectra. Results: Results agreed with those obtained by clinical methods for the following biomolecules when analyzed in the following order: albumin, glucose, fibrinogen, IgG2, lactate, IgG1, α1-antitrypsin, α2-macroglobulin, transferrin, apolipoprotein (Apo)-A1, urea, Apo-B, IgM, Apo-C3, IgA, IgG4, IgG3, IgD, haptoglobin, and α1-acid glycoprotein. Conclusion: FT-IR spectrometry is a useful tool for determining concentrations of several plasma biomolecules.
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Wang, Y., G. J. Heigenhauser i C. M. Wood. "Integrated responses to exhaustive exercise and recovery in rainbow trout white muscle: acid-base, phosphogen, carbohydrate, lipid, ammonia, fluid volume and electrolyte metabolism." Journal of Experimental Biology 195, nr 1 (1.10.1994): 227–58. http://dx.doi.org/10.1242/jeb.195.1.227.
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White muscle and arterial blood plasma were sampled at rest and during 4 h of recovery from exhaustive exercise in rainbow trout. A compound respiratory and metabolic acidosis in the blood was accompanied by increases in plasma lactate (in excess of the metabolic acid load), pyruvate, glucose, ammonia and inorganic phosphate levels, large elevations in haemoglobin concentration and haematocrit, red cell swelling, increases in the levels of most plasma electrolytes, but no shift of fluid out of the extracellular fluid (ECF) into the intracellular fluid (ICF) of white muscle. The decrease in white muscle pHi was comparable to that in pHe; both recovered by 4 h. Creatine phosphate and ATP levels were both reduced by 40% after exercise, the former recovering within 0.25 h, whereas the latter remained depressed until 4 h. Changes in creatine concentration mirrored those in creatine phosphate, whereas changes in IMP and ammonia concentration mirrored those in ATP. White muscle glycogen concentration was reduced 90% primarily by conversion to lactate; recovery was slow, to only 40% of resting glycogen levels by 4 h. During this period, most of the lactate and metabolic acid were retained in white muscle and there was excellent conservation of carbohydrate, suggesting that in situ glycogenesis rather than oxidation was the major fate of lactate. The redox state ([NAD+]/[NADH]) of the muscle cytoplasm, estimated from ICF lactate and pyruvate levels and pHi, remained unchanged from resting levels, challenging the traditional view of the 'anaerobic' production of lactate. Furthermore, the membrane potential, estimated from levels of ICF and ECF electrolytes using the Goldman equation, remained unchanged throughout, challenging the view that white muscle becomes depolarized after exhaustive exercise. Indeed, ICF K+ concentration was elevated. Lactate was distributed well out of electrochemical equilibrium with either the membrane potential (Em) or the pHe-pHi difference, supporting the view that lactate is actively retained in white muscle. In contrast, H+ was actively extruded. Ammonia was distributed passively according to Em rather than pHe-pHi throughout recovery, providing a mechanism for retaining high ICF ammonia levels for adenylate resynthesis in situ. Although lipid is not traditionally considered to be a fuel for burst exercise, substantial decreases in free carnitine and elevations in acyl-carnitines and acetyl-CoA concentrations indicated an important contribution of fatty acid oxidation by white muscle during both exercise and recovery.
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Hoopes, Lisa A., André M. Landry Jr. i Erich K. Stabenau. "Physiological effects of capturing Kemp's ridley sea turtles, Lepidochelys kempii, in entanglement nets". Canadian Journal of Zoology 78, nr 11 (1.11.2000): 1941–47. http://dx.doi.org/10.1139/z00-140.
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Blood samples were collected from 58 wild Kemp's ridley sea turtles (Lepidochelys kempii) to examine the physiological effects of capture in entanglement nets. Captured turtles were placed in holding tanks or in-water cages to examine whether the postcapture holding protocol influenced the time course of recovery of blood homeostasis. Lactate concentrations at capture were 4.5 ± 0.3 and 3.5 ± 0.3 mmol/L (mean ± SE) for L. kempii assigned to the in-water-cage and holding-tank treatments, respectively. Turtles held in holding tanks for 1 h exhibited a significant increase in lactate concentration over capture levels, whereas lactate concentrations in the cage-held animals did not change. Lactate concentrations declined to less than 1.0 mmol/L by 6 and 10 h post capture for turtles in the in-water-cage and holding-tank treatments, respectively. Plasma norepinephrine (NE) and epinephrine (E) concentrations at capture were substantially elevated above base-line levels reported in the literature for comparably sized loggerhead sea turtles (Caretta caretta). Turtles in holding tanks exhibited greater reductions in NE and E at 1 h post capture than did their counterparts in the in-water cages. Although plasma Na+ and Cl- concentrations were not affected by entanglement netting, K+ concentration was elevated in tank-held L. kempii at 1 h post capture. Taken together, these data indicate that entanglement netting causes significant physiological disturbance in sea turtles and that recovery of blood homeostasis is influenced by the postcapture holding protocol.
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Widness, John A., Lance S. Lowe, Edward F. Bell, Leon F. Burmeister, Donald M. Mock, James A. Kistard i Harry Bard. "Adaptive responses during anemia and its correction in lambs". Journal of Applied Physiology 88, nr 4 (1.04.2000): 1397–406. http://dx.doi.org/10.1152/jappl.2000.88.4.1397.
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There is limited information available on which to base decisions regarding red blood cell (RBC) transfusion treatment in anemic newborn infants. Using a conscious newborn lamb model of progressive anemia, we sought to identify accessible metabolic and cardiovascular measures of hypoxia that might provide guidance in the management of anemic infants. We hypothesized that severe phlebotomy-induced isovolemic anemia and its reversal after RBC transfusion result in a defined pattern of adaptive responses. Anemia was produced over 2 days by serial phlebotomy (with plasma replacement) to Hb levels of 30–40 g/l. During the ensuing 2 days, Hb was restored to pretransfusion baseline levels by repeated RBC transfusion. Area-under-the-curve methodology was utilized for defining the Hb level at which individual study variables demonstrated significant change. Significant reciprocal changes ( P < 0.05) of equivalent magnitude were observed during the phlebotomy and transfusion phases for cardiac output, plasma erythropoietin (Epo) concentration, oxygen extraction ratio, oxygen delivery, venous oxygen saturation, and blood lactate concentration. No significant change was observed in resting oxygen consumption. Cardiac output and plasma Epo concentration increased at Hb levels <75 g/l, oxygen delivery and oxygen extraction ratio decreased at Hb levels <60 g/l, and venous oxygen saturation decreased and blood lactate concentration increased at Hb levels <55 g/l. We speculate that plasma Epo and blood lactate concentrations may be useful measures of clinically significant anemia in infants and may indicate when an infant might benefit from a RBC transfusion.
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Lamanca, John J., i Emily M. Haymes. "Effects of Low Ferritin Concentration on Endurance Performance". International Journal of Sport Nutrition 2, nr 4 (grudzień 1992): 376–85. http://dx.doi.org/10.1123/ijsn.2.4.376.
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To determine the effects of depleted iron stores on endurance performance and blood lactate concentration, eight active women with normal (>26 ng/ml) and eight with low (< I2 nglml) plasma ferritin concentrations were studied while performing aand an endurance test (80%) on a cycle ergometer. The low femtin group had significantly lower serum iron concentration and transferrin saturation and higher TIBC than the normal femtin group. Meanwas not significantly different between groups. No significant difference was found in total time to exhaustion during the endurance test for low (23.2 min) and normal (27.0 min) femtin groups; however, the normal femtin group exercised 14% longer. Blood lactate concentrations following the VOzmax and endurance test did not differ significantly between groups. Food diaries revealed lower daily absorbable iron intake by the low femtin group compared to the normal ferritin group. Ferritin concentration was significantly related to absorbable iron (r=.72) and total iron (r=.70) intake. The results suggest that women with depleted iron stores who are not anemic may have less endurance, but do not have higher blood lactate during exercise than women with normal iron stores.
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Moss, M., S. Kurzner, Y. Razlog i G. Lister. "Hypoxanthine and lactate concentrations in lambs during hypoxic and stagnant hypoxia". American Journal of Physiology-Heart and Circulatory Physiology 255, nr 1 (1.07.1988): H53—H59. http://dx.doi.org/10.1152/ajpheart.1988.255.1.h53.
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To determine the suitability of plasma hypoxanthine as a marker of tissue hypoxia, we studied the relationship of arterial plasma hypoxanthine and blood lactate concentrations to the cumulative O2 deficit during hypoxemia and low cardiac output (hypoxic and stagnant hypoxia, respectively). Eight intact, chronically catheterized lambs were studied using ketamine sedation. Comparable reductions in O2 transport and consumption were produced with each form of hypoxia. Lactate was linearly related to O2 deficit during both forms of hypoxia, although the slope of the regression was greater for low cardiac output (0.049) than hypoxemia (0.032). Hypoxanthine was linearly related to cumulative O2 deficit only during low cardiac output. During hypoxemia, hypoxanthine concentration initially increased but plateaued with further increases in O2 deficit. The discrepancy in response of hypoxanthine was most likely caused by differences in the rate of elimination between stagnant and hypoxic hypoxia. We concluded that plasma hypoxanthine concentration was not a reliable marker for tissue hypoxia because it differed with the cause of O2 deprivation and did not necessarily reflect the severity of O2 deprivation.
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Strong, P., R. Anderson, J. Coates, F. Elus, B. Evans, M. F. Gurden, J. Johnstone, I. Kennedy i D. P. Martin. "Suppression of Non-Esterified Fatty Acids and Triacylglycerol in Experimental Animals by the Adenosine Analogue GR79236". Clinical Science 84, nr 6 (1.06.1993): 663–69. http://dx.doi.org/10.1042/cs0840663.
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1. This is the first description of the metabolic activity of a novel adenosine A1-receptor agonist, GR79236. GR79236 inhibited catecholamine-induced lipolysis in human, rat and dog isolated adipocytes. 2. Oral administration of GR79236 (0.1-10 mg/kg) to fed rats induced minimal changes in the plasma concentration of non-esterified fatty acids and in the blood concentrations of glucose and lactate. 3. Intravenous infusion of GR79236 to fasted pithed rats, or oral administration of GR79236 to fasted conscious rats and dogs, produced time- and dose-dependent decreases in the plasma non-esterified fatty acid concentration. In the fasted rats, doses of GR79236 that lowered plasma levels of non-esterified fatty acids also produced hypotriglyceridaemia and anti-ketotic effects. 4. Only in the pithed rats were acute effects on the plasma glucose and lactate concentrations observed. Hypoglycaemia and hyperlactataemia occurred over the dose range studied (1 × 10−11-1 × 10−8 mol min−1 kg−1). 5. This profile of activity suggests that compounds such as GR79236 might be agents which can be used to define the role of excessive lipolysis in experimental (and human) pathophysiology.
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Ponganis, Paul J., Gerald L. Kooyman, Eugene A. Baranov, Philip H. Thorson i Brent S. Stewart. "The aerobic submersion limit of Baikal seals, Phoca sibirica". Canadian Journal of Zoology 75, nr 8 (1.08.1997): 1323–27. http://dx.doi.org/10.1139/z97-756.
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An aerobic dive limit (ADL), the diving duration beyond which postdive lactate concentration increases above the resting level, has been estimated theoretically for many species. Such calculations have been based on an oxygen store/diving metabolic rate (MR) equation. Until now, an ADL has been determined empirically from measurements of blood lactate concentration only in the Weddell seal, Leptonychotes weddellii. We measured post-submergence plasma lactate concentrations during spontaneous voluntary submersions of three captive adult Baikal seals (Phoca sibirica). Two-phase regression analysis revealed a transition in the lactate concentration – submersion duration relationship after the animal had been diving for 15 min. Data collected in prior studies on oxygen stores and submersion metabolic rates of Baikal seals yielded a calculated aerobic limit of 16 min. As in Weddell seals, the empirically determined aerobic limit was very similar to the theoretical limit. Furthermore, most diving durations recorded during recent studies of free-ranging Baikal seals are under this limit. These data support the concept of an ADL and its estimation by means of an oxygen store/diving MR calculation.
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Leypoldt, John K., Mauro Pietribiasi, Anna Ebinger, Michael A. Kraus, Allan Collins i Jacek Waniewski. "Acid–base kinetics during hemodialysis using bicarbonate and lactate as dialysate buffer bases based on the H+ mobilization model". International Journal of Artificial Organs 43, nr 10 (4.03.2020): 645–52. http://dx.doi.org/10.1177/0391398820906524.
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Background: The H+ mobilization model has been recently reported to accurately describe intradialytic kinetics of plasma bicarbonate concentration; however, the ability of this model to predict changing bicarbonate kinetics after altering the hemodialysis treatment prescription is unclear. Methods: We considered the H+ mobilization model as a pseudo-one-compartment model and showed theoretically that it can be used to determine the acid generation (or production) rate for hemodialysis patients at steady state. It was then demonstrated how changes in predialytic, intradialytic, and immediate postdialytic plasma bicarbonate (or total carbon dioxide) concentrations can be calculated after altering the hemodialysis treatment prescription. Results: Example calculations showed that the H+ mobilization model when considered as a pseudo-one-compartment model predicted increases or decreases in plasma total carbon dioxide concentrations throughout the entire treatment when the dialysate bicarbonate concentration is increased or decreased, respectively, during conventional thrice weekly hemodialysis treatments. It was further shown that this model allowed prediction of the change in plasma total carbon dioxide concentration after transfer of patients from conventional thrice weekly to daily hemodialysis using both bicarbonate and lactate as dialysate buffer bases. Conclusion: The H+ mobilization model can predict changes in plasma bicarbonate or total carbon dioxide concentration during hemodialysis after altering the hemodialysis treatment prescription.
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Katz, S. D., B. Bleiberg, J. Wexler, K. Bhargava, J. J. Steinberg i T. H. LeJemtel. "Lactate turnover at rest and during submaximal exercise in patients with heart failure". Journal of Applied Physiology 75, nr 5 (1.11.1993): 1974–79. http://dx.doi.org/10.1152/jappl.1993.75.5.1974.
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Systemic and lower limb skeletal muscle lactate metabolism was studied in 10 men with congestive heart failure by use of a primed continuous intravenous infusion of L-(+)-[U-14C]lactate. Arterial and deep femoral venous blood samples were obtained at rest and during 30 min of submaximal exercise. Systemic lactate metabolic turnover rate (Rd) was determined using Steele's isotopic steady-state equation (Rd = isotopic infusion rate/arterial specific activity). Plasma lactate concentrations in the artery and deep femoral vein did not change significantly from resting values during exercise (1.11 +/- 0.13 vs. 1.26 +/- 0.12 and 1.27 +/- 0.12 vs. 1.30 +/- 0.12 mM, respectively), whereas Rd increased from 22.5 +/- 1.8 to 41.6 +/- 4.8 mumol.kg-1.min-1 (P < 0.005). Rd did not significantly correlate with arterial lactate concentration during rest or exercise. Because of simultaneous uptake and release of lactate in skeletal muscle, arterial and deep femoral venous lactate concentrations are not closely related to either systemic or lower limb skeletal muscle lactate metabolism in patients with congestive heart failure.
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Szucsik, Amanda, Valarie Baliskonis i Kenneth H. McKeever. "Effect of seven common supplements on plasma electrolyte and total carbon dioxide concentration and strong ion difference in Standardbred horses subjected to a simulated race test". Equine and Comparative Exercise Physiology 3, nr 1 (luty 2006): 37–44. http://dx.doi.org/10.1079/ecp200676.
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AbstractThis study used a randomized crossover design, with investigators blind to the treatment given, to test the hypothesis that seven commercially available electrolyte supplements would alter plasma concentrations of Na+, K+, Cl−, lactate, total protein (TP) and total carbon dioxide (tCO2) as well as plasma strong ion difference (SID) and haematocrit (HCT). Ten unfit Standardbred mares (∼450 kg, 4–9 years) completed a series of simulated race exercise tests (SRT) during which venous blood was collected at five sampling intervals (prior to receiving electrolyte treatment, prior to the SRT, immediately following exercise and at 60 and 90 min post-SRT). Plasma electrolyte and tCO2 concentrations were measured in duplicate using a Beckman EL-ISE electrolyte analyser. No difference (P>0.05) between treatments was detected at any of the five sampling intervals for plasma [Na+], [K+], [Cl−] or [tCO2]. Similarly, no significant difference was detected between treatments across each of the five sampling intervals for plasma SID, HCT or TP concentration. There were differences (P<0.05) in plasma [Na+], [K+] and [tCO2] (as well as plasma SID, HCT, and TP concentration) in the immediately post-SRT samples that were attributable to the physiological pressures associated with acute exercise. No differences (P>0.05) were detected between treatments across the pre-electrolyte and pre-SRT sampling intervals for plasma lactate concentration. There was, however, a significant time by treatment interaction during the 0, 60 and 90 min post-SRT sampling intervals for this parameter. The electrolyte supplements featured in this investigation did not affect either plasma tCO2 concentration or SID; however, this result does not rule out the potential for other supplements, especially those containing alkalinizing ingredients, to exert an effect that could push a horse towards threshold values.
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She, Pengxiang, Yingsheng Zhou, Zhiyou Zhang, Kathleen Griffin, Kavitha Gowda i Christopher J. Lynch. "Disruption of BCAA metabolism in mice impairs exercise metabolism and endurance". Journal of Applied Physiology 108, nr 4 (kwiecień 2010): 941–49. http://dx.doi.org/10.1152/japplphysiol.01248.2009.
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Exercise enhances branched-chain amino acid (BCAA) catabolism, and BCAA supplementation influences exercise metabolism. However, it remains controversial whether BCAA supplementation improves exercise endurance, and unknown whether the exercise endurance effect of BCAA supplementation requires catabolism of these amino acids. Therefore, we examined exercise capacity and intermediary metabolism in skeletal muscle of knockout (KO) mice of mitochondrial branched-chain aminotransferase (BCATm), which catalyzes the first step of BCAA catabolism. We found that BCATm KO mice were exercise intolerant with markedly decreased endurance to exhaustion. Their plasma lactate and lactate-to-pyruvate ratio in skeletal muscle during exercise and lactate release from hindlimb perfused with high concentrations of insulin and glucose were significantly higher in KO than wild-type (WT) mice. Plasma and muscle ammonia concentrations were also markedly higher in KO than WT mice during a brief bout of exercise. BCATm KO mice exhibited 43–79% declines in the muscle concentration of alanine, glutamine, aspartate, and glutamate at rest and during exercise. In response to exercise, the increments in muscle malate and α-ketoglutarate were greater in KO than WT mice. While muscle ATP concentration tended to be lower, muscle IMP concentration was sevenfold higher in KO compared with WT mice after a brief bout of exercise, suggesting elevated ammonia in KO is derived from the purine nucleotide cycle. These data suggest that disruption of BCAA transamination causes impaired malate/aspartate shuttle, thereby resulting in decreased alanine and glutamine formation, as well as increases in lactate-to-pyruvate ratio and ammonia in skeletal muscle. Thus BCAA metabolism may regulate exercise capacity in mice.
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Lang, C. H., G. J. Bagby, H. L. Blakesley, J. L. Johnson i J. J. Spitzer. "Plasma glucose concentration determines direct versus indirect liver glycogen synthesis". American Journal of Physiology-Endocrinology and Metabolism 251, nr 5 (1.11.1986): E584—E590. http://dx.doi.org/10.1152/ajpendo.1986.251.5.e584.
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In the present study hepatic glycogenesis by the direct versus indirect pathway was determined as a function of the glucose infusion rate. Glycogen synthesis was examined in catheterized conscious rats that had been fasted 48 h before receiving a 3-h infusion (iv) of glucose. Glucose, containing tracer quantities of [U-14C]- and [6-3H]glucose, was infused at rates ranging from 0 to 230 mumol X min-1 X kg-1. Plasma concentrations of glucose, lactate, and insulin were positively correlated with the glucose infusion rate. Despite large changes in plasma glucose, lactate, and insulin concentrations, the rate of hepatic glycogen deposition (0.46 +/- 0.03 mumol X min-1 X g-1) did not vary significantly between glucose infusion rates of 20 and 230 mumol X min-1 X kg-1. However, the percent contribution of the direct pathway to glycogen repletion gradually increased from 13 +/- 2 to 74 +/- 4% in the lowest to the highest glucose infusion rates, with prevailing plasma glucose concentrations from 9.4 +/- 0.5 to 21.5 +/- 2.1 mM. Endogenous glucose production was depressed (by up to 40%), but not abolished by the glucose infusions. Only a small fraction (7-14%) of the infused glucose load was incorporated into liver glycogen via the direct pathway irrespective of the glucose infusion rate. Our data indicate that the relative contribution of the direct and indirect pathways of hepatic glycogen synthesis are dependent on the glucose load or plasma glucose concentration and emphasize the predominance of the indirect pathway of glycogenesis at plasma glucose concentrations normally observed after feeding.