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PubMed1977

[Acidosis and clinical condition in asphyctic calves].

In depressed calves (modified APGAR score 4-6) there is at birth an evident combined respiratory-metabolic acidosis (pH = 7.082 +/- 0.175; pCO2 = 73.3 +/- 26.8 mm Hg; BE = -10.6 +/- 7.2 mmol/l). The metabolic adaptation is completed after 6 hours, the respiratory acidosis is present up to 24 hours after delivery. In comparison to normal calves there are significant deviations in pH-values, base excess standard bicarbonate and actual bicarbonate during the whole investigation time. The carbon dioxide tensions of the depressed calves are at birth similar to those of normal calves, but in the following hours they are significantly higher. A definite relationship can be demonstrated between the 1 minute APGAR score and pH-value, base excess, standard bicarbonate and actual bicarbonate. Oxygen tension, oxygen saturation and carbon dioxide do not correlate with the clinical condition.

Acidosis↗

PubMed1980

Pancreatic tissue pH in experimental acidosis and alkalosis.

The pH was studied in pancreatic tissue and arterial blood in 22 dogs. Respiratory acidosis was induced by CO2 inhalations in 5 dogs, respiratory alkalosis by hyperventilation in 5 dogs, metabolic acidosis by intravenous(i.v.) infusion of 0.1 N HCl in 5 dogs, metabolic alkalosis by i.v. infusion of 4.2% Na bicarbonate in 5 dogs. The differences between the shifts of blood pH and tissue pH were not significant statistically. Infusion of Ringer's solution failed to affect the pH in blood and pancreatic tissue in two control animals. It is concluded, that with an adequate tissue blood flow the pancreatic tissue pH is uninformative unless the blood pH is known.

Acidosis↗

PubMed1993

Increased osmolal gap in alcoholic acidosis.

We studied a patient with alcoholic acidosis and an increased osmolal gap. Ethyl alcohol and other compounds that are known to increase serum osmolality in alcoholics were not detected. However, the levels of glycerol, acetone, and the acetone metabolites acetol and 1,2-propanediol were increased in the serum of this patient. On admission and 3 and 7 hours after admission, the combined serum osmolality of glycerol, acetone, acetol, and 1,2-propanediol accounted for 48%, 92%, and 62% of the increase in the osmolal gap above the highest normal level of 10 mOsm/kg H2O. The disappearance of the osmolal gap correlated with the correction of the acidosis and the concomitant reduction in serum glycerol and acetone levels. Elevations of endogenous glycerol, acetone, and acetone metabolite levels should now be added as causes for an increased osmolal gap in the alcoholic patient. Ingestion of toxic alcohols can no longer be assumed to be the only cause for an increased osmolal gap in alcoholic patients.

Acid-Base Equilibrium↗

PubMed1978

Proximal renal tubular acidosis: association with familial normaldosteronemic hyperpotassemia and hypertension.

Further investigation of a family with normaldosteronemic hyperpotassemia and low-renin hypertension showed seven members from three generations, who ranged in age from 4 to 56 years, to be affected. Results of earlier studies had established a normally functioning renin-aldosterone system and normal renal handling of potassium. Constant, albeit mild and asymptomatic, metabolic acidosis in all those affected prompted bicarbonate loading in both the propositus and his brother, which revealed a maximal renal tubular excretory capacity for bicarbonate reabsorption at serum levels of 18 mmole/liter and proved proximal renal tubular acidosis (PRTA). Further, a linear increase in urinary fractional potassium excretion accompanied that of bicarbonate in both, as in normal individuals. Dextrose-insulin infusion in the brother failed to reduce hyperpotassemia. These data support the hypothesis that a generalized cell membrane defect that specifically impedes potassium influx (as opposed to an isolated renal tubular defect) underlies this autosomal dominant disorder.

Acidosis, Renal Tubular↗

PubMed1986

Metabolic acidosis. Development in two patients receiving a potassium-sparing diuretic and total parenteral nutrition.

Two patients developed a metabolic acidosis associated with a normal undetermined anion concentration while receiving a potassium-sparing diuretic and total parenteral nutrition. In both cases the metabolic acidosis resolved within one week after discontinuing administration of the diuretic. The use of potassium-sparing diuretics in a patient receiving total parenteral nutrition requires caution and continued monitoring for this potential drug-nutrient interaction.

Acidosis↗

PubMed1976

The effect of acidosis in hypokalemic periodic paralysis.

Metabolic acidosis was produced in two patients with hypokalemic periodic paralysis by the administration of ammonium chloride over a period of three days. The challenging test of glucose and insulin produced a substantially smaller reduction of both serum potassium concentration and muscle strength than when the patients were tested in normal acid-base balance. The findings agree with earlier work on acetazolamide, suggesting that metabolic acidosis provides protection against episodes of muscle weakness in periodic paralysis.

Acetazolamide↗

PubMed1986

Ocular findings in childhood lactic acidosis.

We examined ophthalmologically nine children with lactic acidosis. All showed abnormal ocular findings. Optic atrophy was present in six patients, nystagmus in three, blepharoptosis in one, cataract in one, and limitation on abduction in one. We believe that optic atrophy is the most frequent ocular finding and that nystagmus and ophthalmoplegia are common associations in patients with childhood lactic acidosis.

Acidosis, Lactic↗

PubMed1980

Renal tubular acidosis and sensorineural deafness: an autosomal recessive syndrome.

This is the first known reported case of autosomal recessive syndrome of renal tubular acidosis and sensorineural deafness in the otorhinolaryngological literature. Ten cases in six families have been reported in the pediatric literature. Most cases manifested at birth or soon after with vomiting, dehydration, polydipsia, polyuria, hyposthenuria, and failure to thrive. Renal tubular acidosis is a clinical syndrome of disordered acidification out of proportion to the impairment of glomerular filtration, and is associated with alkaline urine. Sensorineural deafness is variable and, in most cases, present in early childhood.

Acidosis, Renal Tubular↗

PubMed1985

Slow sodium acetate infusion in the correction of metabolic acidosis in premature infants.

The treatment of metabolic acidosis is one of many problems encountered in the premature infant during the first days of life. In this study, 11 infants with gestational ages of no more than 34 weeks were given sodium acetate as a continuous infusion from the first day of life. The daily sodium supply was set at 3 mEq/kg. The arterial serum pH was less than 7.30 in infants at the following ages: 1 to 3 hours, four; 24 hours, two; 48 hours, one; and 72 hours, one. The base deficit was calculated to be less than 5 in four infants at the age of 1 to 3 hours, in one infant at 24 hours, in one infant at 48 hours, and in no infants at 72 hours. The serum sodium concentrations were normal. The continuous infusion of sodium acetate seems to be suitable for the slow correction of metabolic acidosis, and the daily sodium supply of 3 mEq/kg gives a stable serum sodium concentration in the premature infant with a gestational age of no more than 34 weeks.

Acetates↗

PubMed1994

Delayed tumor necrosis factor alpha blockade attenuates pulmonary dysfunction and metabolic acidosis associated with experimental gram-negative sepsis.

OBJECTIVE: To ascertain the effect of delayed tumor necrosis factor alpha (TNF-alpha) on the evolution of systemic and pulmonary injury after the onset of sepsis. DESIGN: Prospective controlled trial. INTERVENTION: Anesthetized swine were made septic with a 1-hour infusion of live Pseudomonas aeruginosa, following which a treatment group received an infusion of anti-TNF-alpha monoclonal antibody (5 mg/kg). Control animals received 0.9% saline. RESULTS: Delayed anti-TNF-alpha treatment had no effect on septic pulmonary hypertension or decline in cardiac output. Late recovery in systemic arterial hypotension was associated with a reversal of arterial acidosis (P < .05 by t test and analysis of variance with Tukey's Studentized Range Test) compared with unprotected septic animals. Septic animals had a significant increase in mean (+/- SEM) plasma lactate levels at 5 hours compared with baseline values (3.8 +/- 0.7 vs 2 +/- 0.4, P < .05), but remained unchanged from baseline following anti-TNF-alpha treatment (1.5 +/- 0.1 vs 1.6 +/- 0.2, not significant). Characteristic septic neutropenia was dramatically reversed by anti-TNF-alpha treatment and was associated with downregulation (P < .05 by t test and analysis of variance) of polymorphonuclear neutrophil (PMN) leukocyte CD18 adhesion receptors and reduction (P < .05 by t test and analysis of variance) in lung PMN sequestration measured by myeloperoxidase activity. The mean (+/- SEM) decrease in bronchoalveolar lavage protein indicated an attenuated permeability injury in anti-TNF-alpha animals (septic animals at 5 hours compared with baseline value, 1044 +/- 270 vs 149 +/- 28 micrograms/mL; control animals at 5 hours compared with baseline value, 217 +/- 83 vs 129 +/- 19 micrograms/mL; P < .05 by t test and analysis of variance). CONCLUSIONS: These data show that delayed anti-TNF-alpha treatment reversed metabolic acidosis associated with sepsis. Furthermore, anti-TNF-alpha treatment reversed septic neutropenia, reduced PMN sequestration, and was associated with attenuated lung injury in a model of fulminant sepsis. This supports evidence of PMN-mediated tissue injury in sepsis and suggests mechanisms for potential therapeutic benefit of anti-TNF-alpha treatment in clinical practice.

Acidosis, Lactic↗

PubMed1996

Improvement of muscular oxidative capacity by training is associated with slight acidosis and ATP depletion in exercising muscles.

Metabolic and mechanical properties of female rat skeletal muscles, submitted to endurance training on a treadmill, were studied by a 60-min in vivo multistep fatigue test. 31P-NMR was used to follow energy metabolism and pH. Mechanical performance was greatly improved in trained muscles. The oxidative capacity of the skeletal muscles was evaluated from the relationship between ADP calculated from the creatine kinase equilibrium and work and from the measure of the rate of phosphocreatine (PCr) resynthesis following exercise. In trained muscles, ADP production was lower per unit of mechanical performance, showing an improvement of oxidative metabolism. However, the PCr resynthesis rate was not modified. Slight acidosis and ATP depletion were observed from the beginning of the fatigue test. These modifications suggest changes of the creatine kinase equilibrium favoring mitochondrial ATP production. Our results indicate that muscle status improvement could be accompanied by ATP depletion and minimal acidosis during contraction; this would be of particular importance for objective evaluation of muscle regeneration processes and of gene therapy in muscle diseases.

Acidosis↗

PubMed1978

Iatrogenic lactic acidosis: association with hypertonic glucose administration in a patient with cancer.

A case of lactic acidosis associated with the administration of hypertonic glucose to a patient with a bulky undifferentiated carcinoma is presented. Characteristic alterations in amino acid concentrations were observed during the period of lactic acidosis. Resolution of the metabolic abnormalities were seen with discontinuation of glucose infusion. Short-term glucose infusion in a 90 minute iv glucose tolerance test resulted in an increase in serum lactate and appropriate changes in serine, ornithine, taurine, alanine, and arginine despite normal hormonal responsiveness.

Acidosis↗

PubMed1992

Lactic acidosis. A presentation of metastatic breast cancer arising in pregnancy.

Lactic acidosis B is a rare metabolic complication of malignancy. It usually is associated with advanced and extensive metastatic disease. The authors report a case in which lactic acidosis was the presenting feature of a previously undiagnosed case of metastatic breast cancer in a pregnant woman and that resolved with successful antineoplastic treatment. The authors review the likely cause and management of the condition.

Acidosis, Lactic↗

PubMed1985

Partial pyruvate decarboxylase deficiency with profound lactic acidosis and hyperammonemia: responses to dichloroacetate and benzoate.

We describe the successful use of sodium benzoate in a neonate with hyperammonemia associated with congenital lactic acidosis caused by a partial deficiency of the E1 component of pyruvate dehydrogenase (PDH); of note, this biochemical disturbance has not been previously described in PDH deficiency. The pyruvate dehydrogenase complex in skin fibroblasts had 48% of normal activity with a deficiency of the E1 component. The infant presented with rapid onset of a severe metabolic lactic acidosis, hyperventilation, hyperammonemia, and coma. At 30 hours of age continuous peritoneal dialysis was started; however, plasma NH3 concentrations remained in the 300-400 micrograms/dl range over the next 12 hours. Sodium benzoate, 250 mg/kg, was infused intravenously with a decrease in plasma ammonia of 25 micrograms/dl/hr. Hippurate was documented in the urine and peritoneal fluid after benzoate therapy. At 10.5 months of age, 50 mg/kg dichloroacetate was administered orally under fasting conditions, which resulted in a 56 and 62% reduction in the serum lactate and pyruvate levels, respectively; after 2 weeks on dichloroacetate his fasting levels were significantly decreased. Fibroblast PDH activity responded similarly to this drug. In our patient sodium benzoate was rapidly effective in producing a decline in plasma ammonia that was associated with clinical improvement. We feel that its use in organic acidemias deserves further evaluation and, furthermore, that any child with suspected PDH deficiency requires a clinical trial of dichloroacetate.

Acidosis↗

PubMed1994

Mitochondrial myopathy with anemia, cardiomyopathy, and lactic acidosis: a distinct late onset mitochondrial disorder.

A 40-year-old woman presented with profound muscle weakness resulting in failure to wean from a ventilator and persistent lactic acidosis after having recovered from a pneumonia complicated by adult respiratory distress syndrome, myocardial infarction, renal failure and shock. She had a 28 year history of chronic anemia and exercise intolerance. Anemia and thrombocytopenia persisted after admission. Nonobstructive hypertrophic cardiomyopathy was present. A stroke-like episode occurred. A mitochondrial myopathy with deficiencies in complexes IV and II was demonstrated, but no DNA defect has yet been found. This patient represents a distinct clinical presentation of a mitochondrial disorder characterized by late onset mitochondrial myopathy, chronic anemia, cardiomyopathy, and lactic acidosis.

Acidosis, Lactic↗

PubMed1982

D-lactic acidosis simulating a hypothalamic syndrome after bowel bypass.

A 36-year-old man had one year of periodic symptoms suggestive of episodic hypothalamic dysfunction: hypersomnia, thirst, ravenous hunger and gorging behavior, pallor, and irritability. However, neuroendocrine testing proved normal. A mild transient acidosis at the onset of his attacks and a history of bowel bypass five years earlier prompted metabolic screening. Markedly increased urinary D-lactic and phenolic acids were present, as were intermittent elevations of plasma D-lactic acid during two symptomatic episodes. Prompt and sustained clinical remission coincided with disappearance of abnormal organic acid excretion during oral antibiotic therapy. D-Lactic acidosis must be considered in the differential diagnosis of otherwise unexplained neurological syndromes, particularly in patients with altered bowel anatomy.

Acidosis↗

PubMed1995

Positron emission tomography and magnetic resonance spectroscopy of cerebral glycolysis in children with congenital lactic acidosis.

Congenital lactic acidosis with neurological symptoms may be due to a variety of disorders of energy metabolism. We investigated whether positron emission tomography (PET) and proton magnetic resonance spectroscopy (1H MRS) are capable of demonstrating specific changes to facilitate diagnosis. A corresponding increase of cerebral lactate (with MRS) and rate of glycolysis (with PET) was observed in 2 children with biochemical evidence of defective mitochondrial respiration. No such increase was noted in a child with lactic acidosis due to stress and exercise but normal respiratory chain activity, and in a control case with an epilepsy syndrome without evidence of primary changes of energy metabolism. The results suggest that defects of oxidative phosphorylation may cause a massive increase of glycolysis to cover energy requirements, with corresponding accumulation of lactate in brain tissue. This mechanism can now be demonstrated in vivo and, with further experience, may potentially be used as a diagnostic marker of respiratory chain disorders in brain tissue.

Acidosis, Lactic↗

PubMed1994

Mitochondrial pyruvate metabolism in liver and kidney during acidosis.

Pyruvate transport and carboxylation have been determined in mitochondria from liver and kidney cortex isolated from Wistar rats with acidosis produced by three different treatments: fasting, exercise and ingestion of ammonium chloride. Fasting for 48 h or swimming for 2 h resulted in an increased rate of CO2 fixation by mitochondria from both organs incubated with pyruvate. This increase was accompanied by a rise in the rate of pyruvate transport in all cases except in mitochondria derived from the kidney of the fasted animals. Acute acidosis produced by the ingestion of ammonium chloride resulted in increases in pyruvate transport and carboxylation in kidney mitochondria, but a drop in pyruvate carboxylation was observed in mitochondria from the liver. The results are discussed in terms of the differential regulation of the mitochondria steps for gluconeogenesis from three carbon precursors in liver and kidney, taking into consideration the hormonal status of the animals and the prevailing available substrates in each condition.

Acidosis↗

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