296 resultados para ACIDOSIS
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Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)
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O objetivo principal deste estudo foi verificar se diferentes formas de indução à acidose interferem na determinação da intensidade do lactato mínimo (LACmin) em corredores de longa distância. Desse modo, 14 corredores de provas fundas do atletismo participaram do estudo. Os atletas realizaram três protocolos: 1) teste incremental em esteira rolante, com incrementos de 1km.h-1 a cada três minutos até a exaustão, para a determinação das intensidades de limiar anaeróbio (OBLA), de limiar aeróbio (Laer), consumo máximo de oxigênio (VO2max) e intensidade de consumo máximo de oxigênio (vVO2max); 2) teste de lactato mínimo em pista de atletismo (LACminp), que consistiu de dois esforços máximos de 233m na pista de atletismo com intervalo de um minuto entre cada repetição, com oito minutos de recuperação passiva, seguido de um teste incremental semelhante ao do protocolo 1; e 3) teste de lactato mínimo em esteira rolante (LACmine), constituído de dois esforços máximos de um minuto e 45 segundos com intervalo de um minuto, na intensidade de 120% da vVO2max, seguido dos mesmos procedimentos do protocolo 2. Foram coletadas amostras de sangue do lóbulo da orelha ao final de cada estágio em todos os protocolos e no 7º minuto de recuperação passiva dos testes de LACmine e LACminp. A análise de variância (ANOVA) mostrou que ocorreram diferenças significativas entre as intensidades de LACmine (13,23 ± 1,78km.h-1) e OBLA (14,67 ± 1,44km.h-1). Dessa maneira, a partir dos resultados obtidos no presente estudo, é possível concluir que a determinação da intensidade correspondente ao lactato mínimo é dependente do protocolo utilizado para a indução à acidose. Além disso, o LACmine subestimou a intensidade correspondente ao OBLA, não podendo ser utilizado para a mensuração da capacidade aeróbia de corredores fundistas.
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Compararam-se os efeitos da ventilação espontânea (V E) e controlada (V C) em equinos submetidos à mudança de decúbito durante anestesia. Dezesseis animais foram equitativamente divididos em dois grupos: V E e V C. Os procedimentos cirúrgicos foram iniciados com os animais em decúbito lateral esquerdo (DLE) e, após 75 minutos, os animais foram reposicionados em decúbito lateral direito (DLD). Análises hemogasométricas do sangue arterial foram realizadas após 30 e 75 minutos com os animais posicionados em cada decúbito (M1 e M2 no DLE e M3 e M4 no DLD, respectivamente). Durante a V E, observaram-se hipercapnia (PaCO2 >45mmHg), acidose respiratória (pH <7,35), redução significativa da oxigenação sanguínea após 75min da mudança de decúbito (M4: 205,8±124,7mmHg) em relação aos valores de PaO2 observados antes da mudança de posicionamento (M1: 271,8±84,8mmHg). A Vc foi associada a valores de PaCO2 e pH mais próximos da normalidade bem como resultou em valores de PaO2 significativamente maiores (52 a 96% de elevação nos valores médios) que a V E. Conclui-se que a mudança de decúbito, em equinos anestesiados com halotano e mantidos sob V E, resulta em hipercapnia, acidose respiratória e diminuição dos valores de PaO2. A instituição de V C, desde o início da anestesia, previne a acidose respiratória, além de resultar em valores de PaO2 mais próximos do ideal para animais respirando O2 a 100%.
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O presente trabalho objetivou avaliar a função renal de dez cães adultos saudáveis submetidos à administração de doses terapêuticas do antifúngico anfotericina B, cuja utilização tem sido limitada pelo seu elevado potencial nefrotóxico, e avaliar o método laboratorial mais sensível e precoce de diagnóstico de lesão renal. Foram realizadas, diariamente, urinálise, excreção fracionada de sódio e potássio, dosagem sérica de creatinina e uréia e atividade urinária de gama-glutamiltransferase (GGT). Concluiu-se que a anfotericina B provoca lesões nos túbulos proximal e distal, induzindo acidose tubular renal do tipo I e Diabetes insipidus nefrogênico em cães. Avaliação da função renal, preferencialmente por dosagens de creatinina, uréia e potássio séricos, é recomendada antes de cada aplicação do fármaco. A densidade urinária foi o parâmetro mais precocemente alterado pela lesão renal. A GGT urinária não foi eficaz para o diagnóstico precoce de lesão induzida por anfotericina B.
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A desnutrição protéico-energética constitui problema comum aos pacientes com insuficiência renal crônica, influenciando diretamente na sua morbi-mortalidade. A acidose metabólica tem papel no catabolismo protéico, ativando a via proteolítica proteasoma-ubiquitina, dependente de adenosina trifosfato, e conjuntamente com glicocorticóides induz uma maior atividade na desidrogenase que degrada os aminoácidos de cadeia ramificada. Esta revisão teve como objetivo descrever o mecanismo pelo qual a acidose metabólica nos pacientes com insuficiência renal crônica promove o catabolismo protéico, favorecendo assim a desnutrição, bem como avaliar os efeitos do uso de bicarbonato de sódio na correção da acidose e conseqüentemente redução do catabolismo protéico. Pesquisas mostram melhora da acidose pelo uso de bicarbonato de sódio e conseqüente redução do catabolismo protéico na insuficiência renal crônica, podendo ser esta uma conduta promissora na atenuação da desnutrição nestes pacientes.
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The equilibrium point between blood lactate production and removal (La-min(-)) and the individual anaerobic threshold (IAT) protocols have been used to evaluate exercise. During progressive exercise, blood lactate [La-](b), catecholamine and cortisol concentrations, show exponential increases at upper anaerobic threshold intensities. Since these hormones enhance blood glucose concentrations [Glc](b), this study investigated the [Glc] and [La-](b) responses during incremental tests and the possibility of considering the individual glucose threshold (IGT) and glucose minimum;(Glc(min)) in addition to IAT and La-min(-) in evaluating exercise. A group of 15 male endurance runners ran in four tests on the track 3000 m run (v(3km)); IAT and IGT- 8 x 800 m runs at velocities between 84% and 102% of v(3km); La-min(-) and Glc(min) - after lactic acidosis induced by a 500-m sprint, the subjects ran 8 x 800 m at intensities between 87% and 97% of v(3km); endurance test (ET)- 30 min at the velocity of IAT. Capillary blood (25 mu l) was collected for [La-](b) and [Glc](b) measurements. The TAT and IGT were determined by [La-](b) and [Glc](b) kinetics during the second test. The La-min(-) and Glc(min) were determined considering the lowest [La-] and [Glc](b) during the third test. No differences were observed (P < 0.05) and high correlations were obtained between the velocities at IAT [283 (SD 19) and IGT 281 (SD 21)m. min(-1); r = 0.096; P < 0.001] and between La,, [285 (SD 21)] and Glc(min) [287 (SD 20) m. min(-1) = 0.77; P < 0.05]. During ET, the [La-](b) reached 5.0 (SD 1.1) and 5.3 (SD 1.0) mmol 1(-1) at 20 and 30 min, respectively (P > 0.05). We concluded that for these subjects it was possible to evaluate the aerobic capacity by IGT and Glc(min), as well as by IAT and La-min(-).
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Water, compared with plasma at a pH of 7.4, is a weak acid. The addition of free water to a patient should have an acidifying effect (dilutional acidosis) and the removal of it, an alkalinizing effect (concentrational alkalosis). The specific effects of free water loss or gain in a relatively complex fluid such as plasma has, to the authors' knowledge, not been reported. This information would be useful in the interpretation of the effect of changes in free water in patients. Plasma samples from goats were either evaporated in a tonometer to 80% of baseline volume or hydrated by the addition of distilled water to 120% of baseline volume. The pH and partial pressure of carbon dioxide, sodium, potassium, ionized calcium, chloride, lactate, phosphorous, albumin, and total protein concentrations were measured. Actual base excess (ABE), standard bicarbonate, anion gap, strong ion difference, strong ion gap, unmeasured anions, and the effects of sodium, chloride, phosphate, and albumin changes on ABE were calculated. Most parameters changed 20% in proportion to the magnitude of dehydration or hydration. Bicarbonate concentration, however, increased only 11% in the evaporation trial and decreased only -2% in the dehydration trial. The evaporation trial was associated with a mild, but significant, metabolic alkalotic effect (ABE increased 3.2 mM/L), whereas the hydration trial was associated with a slight, insignificant metabolic acidotic effect (ABE decreased only 0.6 mM/L). The calculated free water ABE effect (change in sodium concentration) was offset by opposite changes in calculated chloride, lactate, phosphate, and albumin ABE effects.
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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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Aim. The aim of the present study was to investigate the validity of the Lactate Minimum Test (LMT) for the determination of peak VO2 on a cycle ergometer and to determine the submaximal oxygen uptake (VO2) and pulmonary ventilation (VE) responses in an incremental exercise test when it is preceded by high intensity exercise (i.e., during a LMT).Methods. Ten trained male athletes (triathletes and cyclists) performed 2 exercise tests in random order on an electromagnetic cycle ergometer: 1) Control Test (CT): an incremental test with an initial work rate of 100 W, and with 25 W increments at 3-min intervals, until voluntary exhaustion; 2) LMT: an incremental test identical to the CT, except that it was preceded by 2 supramaximal bouts of 30-sec (similar to120% VO(2)peak) with a 30-sec rest to induce lactic acidosis. This test started 8 min after the induction of acidosis.Results. There was no significant difference in peak VO2 (65.6+/-7.4 ml.kg(-1).min(-1); 63.8+/-7.5 ml.kg(-1).min(-1) to CT and LMT, respectively). However, the maximal power output (POmax) reached was significantly higher in CT (300.6+/-15.7 W) than in the LMT (283.2+/-16.0 W).VO2 and VE were significantly increased at initial power outputs in LMT.Conclusion. Although the LMT alters the submaximal physiological responses during the incremental phase (greater initial metabolic cost), this protocol is valid to evaluate peak VO2, although the POmax reached is also reduced.
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A combination of 0.5 mg/kg of methotrimeprazine, 0.1 mg/kg of midazolam and 100 mg/kg of a 10 per cent guaiphenesin solution was investigated for the induction of recumbency in 15 horses; the addition of 1.6 mg/kg of ketamine was also evaluated in 15 horses and anaesthesia was maintained with halothane in oxygen. The horses became recumbent quickly and smoothly and they recovered quietly, with little ataxia. Tachycardia occurred after induction, but no other changes from pre-operative values were observed until halothane in oxygen had been given, when hypothermia, hypotension, bradypnoea, hyperoxaemia, respiratory acidosis and decreased respiratory minute volume developed. Horses given ketamine in addition to methotrimeprazine, midazolam and guaiphenesin were easier to intubate and recovered more quickly than horses receiving only methotrimeprazine, midazolam and guaiphenesin.
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The authors studied the effect of temperature and humidity of inhaled gases on the respiratory tract of dogs submitted to mechanic ventilation. According to these two variables, fourty dogs were divided in five groups: -G1: 22-26°C and 17-20 mg H2O.l-1; G2: 27-31°C and 23-27 mg H2O.l-1; G3: 32-36°C and 30-36 mg H2O.l-1; G4: 37-41°C and 40-49 mg H2O.l-1; G5: 42-46°C and 59-65 mg H2O.l-1. The following parameters were evaluated: medial arterial pressure, cardiac frequency, venous pressure of inferior cava (CVP), endotracheal pressure, arterial pH, PaO2, PaCO2, rectal temperature, and the histology of the tracheobronchial tree. In the groups G1 and G5, the endotracheal pressure and CVP presented a slight raise. In the groups G1, G2 and G3, there was no histological modification or progressive hypothermia. The group G5 presented metabolic acidosis and great histological alteration; in this group the rectal temperature remained stable. The group G4 presented great histological alteration and hypothermia. In conclusion, the temperature and humidity of inhaled gases should not be higher than 36°C and 36 mm H2O.l-1, respectively. However, the stability of body temperature only is achieved when the temperature of the inhaled air is 42°C or higher.
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Glucose was infused intravenously into six ponies during halothane anaesthesia, to evaluate its effect on their endocrine response to anaesthesia. The ponies were premedicated with acepromazine, and anaesthesia was induced with thiopentone and maintained with halothane in oxygen for two hours. Glucose was infused to maintain the plasma glucose concentration above 20 mmol/litre. Anaesthesia was associated with hypothermia, a decrease in haematocrit, hypotension, hyperoxaemia, respiratory acidosis and an increase in the plasma concentrations of lactate and arginine vasopressin. The concentration of β-endorphin in plasma increased transiently after 20 minutes but there were no changes in concentrations of adrenocorticotrophic hormone, dynorphin, cortisol or catecholamines. These data suggest that the glucose infusion attenuated the normal adrenal response of ponies to halothane anaesthesia.
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β-Adrenoreceptor blockade is reported to impair endurance, power output and work capacity in healthy subjects and patients with hypertension. The purpose of this study was to investigate the effect in eighth athletic males of an acute β-adrenergic blockade with propranolol on their individual power output corresponding to a defined lactate minimum (LM). Eight fit males (cyclist or triathlete) performed a protocol to determine the power output corresponding to their individual LM (defined from an incremental exercise test after a rapidly induced exercise lactic acidosis). This protocol was performed twice in a double-blind randomized order by each athlete first ingesting propranolol (80mg) and in a second trial a placebo, 120 minutes respectively prior to the test sequence. The blood lactate concentration obtained 7 minutes after anaerobic exercise (a Wingate test) was significantly lower after acute β-adrenergic blockade (8.6 ± 1.6mM) than under the placebo condition (11.7 ± 1.6mM). The work rate at the LM was lowered from 215.0 ± 18.6 to 184.0 ± 18.6 watts and heart rate at the LM was reduced from 165 ± 1.5 to 132 ± 2.2 beats/minute as a result of the blockade. There was a non-significant correlation (r = 0.29) between the power output at the LM with and without acute β-adrenergic blockade. In conclusion, since the intensity corresponding to the LM is related to aerobic performance, the results of the present study, are able to explain in part, the reduction in aerobic power output produced during β-adrenergic blockade.
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The present work shows laboratory aspects, electrocardiogram and histopathology results during experimental envenomation by Crotalus durissus terrificus in dogs treated with antiophidic serum. Twenty-one dogs were divided into three groups of seven animals each. Group I received 1mg/kg venom (sc); Group II received 1mg/kg venom (sc), 50mg antiophidic serum (iv) and fluid therapy including 0.9% NaCl solution (iv); and Group III received 1mg/kg venom (sc), 50mg antiophidic serum (iv) and fluid therapy including 0.9% NaCl solution containing sodium bicarbonate diluted to the dose of 4mEq/kg. Urinalysis showed brown urine, proteinuria, occult blood and myoglobinuria. Respiratory acidosis and hypotension were also observed. At the venom inoculation site, there was discreet edema, popliteal lymph node response, musculature presenting whitish areas and necrotic myositis with myoregenerative activity. There was not evidence of electrocardiographical and biochemical alterations.