908 resultados para Lactate minimum
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Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)
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Increased fighting is an effect of desynchronized sleep deprivation (DSD) in rats, and recently this behavior has been suggested to be spontaneous panic and equivalent to panic disorder. In the present study we tested this hypothesis by evaluating the effect of sodium lactate on this aggressiveness, because this substance is recognized to induce spontaneous panic attacks in patients. A total of 186 male albino Wistar rats, 250-350 g, 90-120 days of age, were submitted to DSD (multiple platform method) for 0, 4, or 5 days. At the end of the deprivation period the rats were divided into subgroups respectively injected intraperitoneally with 1.86, 2.98 and 3.72 g/kg of 1 M sodium lactate, or 1.86 and 3.72 g/kg of 2 M sodium lactate. The control animals were submitted to the same procedures but received equivalent injections of sodium chloride. Regardless of DSD time, sleep-deprived animals that received sodium lactate presented a significantly higher mean number of fights (0.13 ± 0.02 fights/min) and a longer mean time spent in confrontation (2.43 ± 0.66 s/min) than the controls (0.01 ± 0.006 fights/min and 0.12 ± 0.07 s/min, respectively; P<0.01, Student t-test). For the sodium lactate group, concentration of the solution and time of deprivation increased the number of fights, with the mean number of fights and mean duration of fighting episodes being greater with the 2.98 g/kg dose using 1 M lactate concentration. These results support the hypothesis that fighting induced by DSD is probably a spontaneous panic manifestation. However, additional investigations are necessary in order to accept this as a promising animal model for studies on panic disorder.
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Estudaram-se os efeitos do óxido nitroso (N2O) sobre a concentração alveolar mínima (CAM) do desfluorano. Trinta cães foram distribuídos em dois grupos: desfluorano (GD) e N2O e desfluorano (GDN). Os do GD receberam propofol (8,9±1,65mg/kg) para intubação orotraqueal e após, 11,5V% de desfluorano em 100% de O2. Após 30 minutos, os animais receberam estímulo elétrico e não havendo reação do animal, reduziu-se a concentração em 1,5V%. Repetiu-se o protocolo a cada 15 minutos, cessando-se os estímulos quando observada reação voluntária. Os GDN foram submetidos ao mesmo protocolo, substituindo-se o fluxo diluente por 30% O2 e 70% N2O. Mensuraram-se freqüências cardíaca (FC) e respiratória (FR), pressões arteriais sistólica, diastólica e média (PAS, PAD e PAM), concentração de dióxido de carbono ao final da expiração (ETCO2), saturação de oxihemoglobina (SpO2), temperatura corpórea (TC) e a CAM do desfluorano. Observou-se aumento da FC, ETCO2 e SpO2, e redução da FR e da TC concomitantemente à administração da maior dose de desfluorano, além de redução da CAM do desfluorano. As pressões arteriais diminuíram em M30 aumentando posteriormente. Concluiu-se que o N2O associado ao desfluorano reduz em 16% a CAM do anestésico volátil. Além disso, essa associação promoveu aumento da FC e depressão respiratória.
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OBJECTIVE: To assess the hemodynamic and vasodilating effects of milrinone lactate (ML) in patients with dilated cardiomyopathy (DCM) and New York Heart Association (NYHA) class III and IV heart failure. METHODS: Twenty patients with DCM and NYHA class III and IV heart failure were studied. The hemodynamic and vasodilating effects of ML, administered intravenously, were evaluated. The following variables were compared before and during drug infusion: cardiac output (CO) and cardiac index (CI); pulmonary capillary wedge pressure (PCWP); mean aortic pressure (MAP); mean pulmonary artery pressure (MPAP); mean right atrial pressure (MRAP); left ventricular systolic and end-diastolic pressures (LVSP and LVEDP, respectively); peak rate of left ventricular pressure rise (dP/dt); systemic vascular resistance (SVR); pulmonary vascular resistance (PVR); and heart rate (HR). RESULTS: All patients showed a significant improvement of the analysed parameters of cardiac performance with an increase of CO and CI; a significant improvement in myocardial contractility (dP/dt) and reduction of the LVEDP; PCWP; PAP; MAP; MRAP; SVR; PVR. Were observed no significant increase in HR occurred. CONCLUSION: Milrinone lactate is an inotropic dilating drug that, when administered intravenously, has beneficial effects on cardiac performance and myocardial contractility. It also promotes reduction of SVR and PVR in patients with DCM and NYHA class III and IV of heart failure.
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The results of photometric observations of comet/steroid 2060 Chiron at the Observatorio do Pico dos Dias (Brazil - OPD) and the Observatoire de Haute-Provence (France - OHP) during 1994 and 1995 are presented. The analysis of the data shows a decrease of 2060. Chiron brightness from its peak values of 1988-1991. The absolute magnitude, H-V, varies from a maximum of 6.6 in February 1994 up to a minimum of 6.8 in June 1995. Therefore 2060 Chiron is back to a minimum of activity close to that of 1983-1985. The slope parameter G is found to be G = 0.71 +/- 0.15. It is suggested that the H-G magnitude system, generally adopted to present 2060 Chiron brightness, is not the most appropriate due to the cometary activity of this object. Copyright (C) 1996 Elsevier B.V. Ltd.
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Six Welsh gelding ponies were premedicated with 0.03 mg/kg of acepromazine intravenously (i.v.) prior to induction of anaesthesia with midazolam at 0.2 mg/kg and ketamine at 2 mg/kg i.v.. Anaesthesia was maintained for 2 h using 1.2% halothane concentration in oxygen. Heart rate, electrocardiograph (EGG), arterial blood pressure, respiratory rate, blood gases, temperature, haematocrit, plasma arginine vasopressin (AVP), dynorphin, beta-endorphin, adrenocorticotropic hormone (ACTH), cortisol, dopamine, noradrenaline, adrenaline, glucose and lactate concentrations were measured before and after premedication, immediately after induction, every 20 min during anaesthesia, and at 20 and 120 min after disconnection. Induction was rapid, excitement-free and good muscle relaxation was observed. There were no changes in heart and respiratory rates, Decrease in temperature, hyperoxia and respiratory acidosis developed during anaesthesia and slight hypotension was observed (minimum value 76 +/- 10 mm Hg at 40 mins), No changes were observed in dynorphin, beta-endorphin, ACTH, catecholamines and glucose, Plasma cortisol concentration increased from 220 +/- 17 basal to 354 +/- 22 nmol/L at 120 min during anaesthesia; plasma AVP concentration increased from 3 +/- 1 basal to 346 +/- 64 pmol/L at 100 min during anaesthesia and plasma lactate concentration increased from 1.22 +/- 0.08 basal to 1.76 +/- 0.13 mmol/L at 80 min during anaesthesia, Recovery was rapid and uneventful with ponies taking 46 +/- 6 min to stand. When midazolam/ketamine was compared with thiopentone or detomidine/ketamine for induction before halothane anaesthesia using an otherwise similar protocol in the same ponies, it caused slightly more respiratory depression, but less hypotension. Additionally, midazolam reduced the hormonal stress response commonly observed during halothane anaesthesia and appears to have a good potential for use in horses.
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The objective of this study was to determine the critical speed (CS) for track cycling and to assess whether a lactate steady state occurs at this speed. Fourteen competitive cyclists performed the following tests on an official cycling track (333.3 m): 1) incremental test for determination of the intensity corresponding to 4 mM of blood lactate (onset of blood lactate accumulation, OBLA) and maximal oxygen uptake (VO(2)max); 2) CS: 3 maximal bouts for distances of 2, 4 and 6 km executed in random order and with a period of recovery of 40 to 50 min between bouts. CS was determined for each subject from the linear regression between the distance and the time taking to cycle it; 3) Endurance test in which subjects were instructed to pedal at 100% of their individually determined CS for 30 min. At the 10(th) and 30(th) min (or upon exhaustion), 25 mul of blood were collected from ear lobe for later analysis of blood lactate [Lac]b. An increase less than or equal to1 mM between 10 and 30 min of exercise was considered as the criterion for the occurrence of the lactate steady state. CS (49.6 +/- 8.6 ml.kg(-1).min(-1); 36.9 +/- 2.7 km.h(-1)) was significantly higher than OBLA (43.7 8.0 ml.kg(-1).min(-1); 35.24 +/- 2.6 km.h(-1)) although the two parameters were highly correlated (r=0.97). During the endurance test, only 8 of the 14 subjects completed the 30 min period at CS. of these 8 subjects, only 2 presented a lactate steady state. Time to exhaustion at CS was 20.3 +/- 1.6 min for the remaining 6 subjects. The 12 subjects who did not reach a lactate steady state presented mean [Lac]b values of 7.4 +/- 1.3 mM at 10 min and of 9.4 +/- 1.9 mM at the end of the test (exhaustion), characterizing an exercise intensity of high lactacidemia. on the basis of the present results, we can conclude that CS determined by a track cycling test seems to overestimate the intensity of the maximal lactate steady state for most subjects.
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1. Maximal lactate steady state (MLSS) corresponds to the highest blood lactate concentration (MLSSc) and workload (MLSSw) that can be maintained over time without continual blood lactate accumulation and is considered an important marker of endurance exercise capacity. The present study was undertaken to determine MLSSw and MLSSc in running mice. In addition, we provide an exercise training protocol for mice based on MLSSw.2. Maximal lactate steady state was determined by blood sampling during multiple sessions of constant-load exercise varying from 9 to 21 m/min in adult male C57BL/6J mice. The constant-load test lasted at least 21 min. The blood lactate concentration was analysed at rest and then at 7 min intervals during exercise.3. The MLSSw was found to be 15.1 +/- 0.7 m/min and corresponded to 60 +/- 2% of maximal speed achieved during the incremental exercise testing. Intra- and interobserver variability of MLSSc showed reproducible findings. Exercise training was performed at MLSSw over a period of 8 weeks for 1 h/day and 5 days/week. Exercise training led to resting bradycardia (21%) and increased running performance (28%). of interest, the MLSSw of trained mice was significantly higher than that in sedentary littermates (19.0 +/- 0.5 vs 14.2 +/- 0.5 m/min; P = 0.05), whereas MLSSc remained unchanged (3.0 mmol/L).4. Altogether, we provide a valid and reliable protocol to improve endurance exercise capacity in mice performed at highest workload with predominant aerobic metabolism based on MLSS assessment.
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The aim of this study was to determine the effect of exercise mode on the blood lactate removal during recovery of high-intensity exercise. Nine male individuals performed the following tests in order to determine the blood lactate removal: Running - 2x200 m, the subjects ran at their maximum capacity, and rested 2 min between each bout. Swimming - 2x50 m, the subjects swam at their maximum capacity, and rested 2 min between each bout. Each test was realized on different days with three recovery modes: passive (sitting down), swimming, or running. Recovery exercise intensity was corresponding to the aerobic threshold. All recovery activities lasted 30 min. The two forms of active recovery were initiated 2 min after the end of high-intensity exercise and lasted 15 min, and were followed by 13 min of seated rest. After 1,7, 12,17, and 30 min of the end of high-intensity exercise, blood samples (25 mu l) were collected in order to determine the blood lactate concentration. By linear regression, between the logarithm of lactate concentration and its respective time of recovery, the half-time of blood lactate removal (t1/2) was determined. Time of high-intensity exercise and the lactate concentration obtained in the 1(st) min of recovery were not different between running and swimming. Passive recovery (PR) following running (R-PR=25.5+/-4.3 min) showed a t1/2 significantly higher than PR after swimming (S-PR=18.6+/-4.3 min). The t1/2 of the sequences running-running (R-R=13.0 min), running-swimming (R-S=12.9+/-3.8 min), swimming-swimming (S-S=13.2+/-2.8 min), and swimming-running (S-R=12.9+/-3.8 min) were significantly lower than the t1/2 of the R-PR and S-PR. There was no difference between the t1/2 of the sequences R-R R-S, and S-S. on the other hand the sequence S-R showed a t1/2 significantly lower than the sequences S-S and R-R. It was concluded that the two forms of active recovery determine an increase in the blood lactate removal, regardless of the mode of high-intensity exercise performed previously. Active recovery performed by the muscle groups that were not previously fatigued, can improve the blood lactate removal.
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Introduction - the aim of this study was to analyze the validity of the critical speed (CS) to determine the speed corresponding to 4 mmol 1(-1) of blood lactate (S4) and the speed in a 30 min test (S30min) of swimmers aged 10-15 years.Synthesis of facts - CS, S4 and S30min were determined in 12 swimmers (eight boys and four girls) divided into two groups: 10-12 years and 13-15 years.Conclusion - CS was a good predictor of aerobic performance (S30min) independent of the chronological age, providing practical information about the aerobic performance state of young swimmers. (C) 2002, Editions scientifiques et medicates, Elsevier SAS. All rights reserved.
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Aim. The objective of this study was to verify the effects of active (AR) and passive recovery (PR) after a judo match on blood lactate removal and on performance in an anaerobic intermittent task (4 bouts of upper body Wingate tests with 3-min interval between bouts; 4WT).Methods. The sample was constituted by 17 male judo players of different competitive levels: A) National (Brazil) and International medallists (n. 5). B) State (São Paulo) medallists (n. 7). Q City (São Paulo) medallists (n. 5). The subjects were submitted to: 1) a treadmill test for determination of VO2peak and velocity at anaerobic threshold (VAT); 2) body composition; 3) a 5-min judo combat, 15-min of AR or PR followed by 4WT.Results. The groups did not differ with respect to: body weight, VO2peak, VAT, body fat percentage, blood lactate after combats. No difference was observed in performance between AR and PR, despite a lower blood lactate after combat (10 and 15 min) during AR compared to PR. Groups A and B performed better in the high-intensity intermittent exercise compared to athletes with lower competitive level (C).Conclusion. The ability to maintain power output during intermittent anaerobic exercises can discriminate properly judo players of different levels. Lactate removal was improved with AR when compared to PR but AR did not improve performance in a subsequent intermittent anaerobic exercise.
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The maximal lactate steady state (MLSS) is defined as the highest blood lactate concentration that can be maintained over time without a continual blood lactate accumulation. The objective of the present study was to analyze the effects of pedal cadence (50 vs. 100 rev min(-1)) on MLSS and the exercise workload at MLSS (MLSSworkload) during cycling. Nine recreationally active males (20.9 +/- 2.9 years, 73.9 +/- 6.5 kg, 1.79 +/- 0.09 m) performed an incremental maximal load test (50 and 100 rev min(-1)) to determine anaerobic threshold (AT) and peak workload (PW), and between two and four constant submaximal load tests (50 and 100 rev min(-1)) on a mechanically braked cycle ergometer to determine MLSSworkload and MLSS. MLSSworkload was defined as the highest workload at which blood lactate concentration did not increase by more than 1 mM between minutes 10 and 30 of the constant workload. The maximal lactate steady state intensity (MLSSintensity) was defined as the ratio between MLSSworkload and PW. MLSSworkload (186.1 +/- 21.2 W vs. 148.2 +/- 15.5 W) and MLSSintensity (70.5 +/- 5.7% vs. 61.4 +/- 5.1%) were significantly higher during cycling at 50 rev min(-1) than at 100 rev min(-1), respectively. However, there was no significant difference in MLSS between 50 rev min(-1) (4.8 +/- 1.6 mM) and 100 rev min(-1) (4.7 +/- 0.8 mM). We conclude that MLSSworkload and MLSSintensity are dependent on pedal cadence (50 vs. 100 rev min(-1)) in recreationally active individuals. However, this study showed that MLSS is not influenced by the different pedal cadences analyzed.
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Lactate is a compound produced by the anaerobic metabolism of glucose, and hyperlactataemia occurs when the rate of production of lactate exceeds the rate of elimination. This occurs in situations of hypoxia and tissue hypoperfusion. Lactate has been considered a useful prognostic indicator in critically ill patients. Pyometra is a disease of adult female dogs characterized by inflammation of the uterus with an accumulation of exudate, which occurs during the luteal phase. It is one of the most common diseases that occur in the genital tract of female dogs. A total of 31 dogs were diagnosed with pyometra. The diagnosis was confirmed at ultrasonography. of the 31 dogs, 25 females had open cervix pyometra and six had closed cervix pyometra. Plasma lactate concentrations were determined by an enzymatic colorimetric method. The average concentration (+/- SD) of plasma lactate in all 31 bitches with pyometra was 3.55 +/- 0.46 mm. Healthy dogs had plasma lactate concentrations between 0.3 and 2.5 mm (mean +/- SD). Concentrations ranged from 0.8 to 2.9 mm when plasma lactate was measured with a portable device and 0.42.6 mm with the blood gas analyser. Even though plasma lactate values vary between several studies and equipment used to measure concentrations, our results for dogs with pyometra are higher indicating hyperlactataemia (Thorneloe et al. , Can Vet J 48, 283288). Plasma lactate in dogs with closed cervix pyometra was mean +/- SD and in dogs with open cervix pyometra, it was mean +/- SD. The plasma lactate concentration in dogs with pyometra was higher than in healthy bitches, and there was no influence of patency of the cervix on the concentration of plasma lactate concentrations. Plasma lactate concentrations were similar for animals with open and closed pyometra (3.54 +/- 0.52 to 3.64 +/- 1.03 mm).
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Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)