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PubMed1991

Variations in the kinetic response of several different phosphate-dependent glutaminase isozymes during acute metabolic acidosis.

We describe the kinetic modifications to mitochondrial-membrane-bound phosphate-dependent glutaminase in various types of rat tissue brought about by acute metabolic acidosis. The activity response of phosphate-dependent glutaminase to glutamine was sigmoidal, showing positive co-operativity, the Hill coefficients always being higher than 2. The enzyme from acidotic rats showed increased activity at subsaturating concentrations of glutamine in kidney tubules, as might be expected, but not in brain, intestine or liver tissues. Nevertheless, when brain and intestine from control rats were incubated in plasma from acutely acidotic rats enzyme activity increased at 1 mM glutamine in the same way as in kidney cortex. The enzyme from liver tissue remained unaltered. S0.5 and nH values decreased significantly in kidney tubules, enterocytes and brain slices preincubated in plasma from acidotic rats. The sigmoidal curves of phosphate-dependent glutaminase shifted to the left without any significant changes in Vmax. The similar response of phosphate-dependent glutaminase to acute acidosis in the kidney, brain and intestine confirms the fact that enzymes from these tissues are kinetically identical and reaffirms the presence of an ammoniagenic factor in plasma, either produced or concentrated in the kidneys of rats with acute acidosis.

Acidosis↗
PubMed1987

Bicarbonate haemodialysis: an adequate treatment for lactic acidosis in diabetics treated by metformin.

Lactic acidosis in diabetics on metformin therapy is rare but still associated with poor prognosis. The authors report here five cases. Three patients were initially with a cardiovascular collapse and all had an acute renal failure. Sodium bicarbonate haemodialysis therapy led to a dramatic improvement. Consciousness and hemodynamic status recovered rapidly. Severe metabolic and blood gases derangements were also rapidly corrected. Plasma metformin removal, appreciated by repeated blood samplings in 3 cases, was satisfactory. All patients survived. However, blood metformin levels remained abnormally high at the end of the dialytic therapy. In conclusion, (1) bicarbonate dialysis is an adequate treatment of lactic acidosis observed in diabetic patients treated with metformin since it rapidly corrects the acid-base disorders and partially removes metformin; (2) the sole accumulation of metformin is not sufficient to explain lactic acidosis since this latter might be corrected in spite of persisting high levels of blood metformin.

Acidosis, Lactic↗
PubMed1996

The acute reversal of a diet-induced metabolic acidosis does not restore endurance capacity during high-intensity exercise in man.

The present experiment was designed to investigate whether a diet-induced metabolic acidosis was a major factor in the earlier onset of fatigue during high-intensity exercise. Six healthy males cycled to exhaustion at a workload equivalent to 95 percent of maximum oxygen uptake on four separate occasions. Exercise tests were performed after an overnight fast and each test was preceded by one of four experimental conditions. Two experimental diets were designed, either to replicate each subject's own normal diet [N diet, mean (SD) daily energy intake (E) = 13 (0.7) MJ, 14.5 (0.8) percent protein (Pro), 37.5 (2.2) percent fat (Fat) and 47.5 (2.1) percent carbohydrate (CHO)], or a low-carbohydrate diet [E = 12.6 (0.8) MJ, 33.6 (1.3) percent Pro, 64.4 (1.5) percent Fat and 2.2 (0.4) percent CHO]. These diets were prepared and consumed within the department over a 3-day period. Over a 3-period prior to the exercise trial subjects ingested either NaHCO(3) or CaCO(3) (3.6 and 3.0 mmol*kg body mass), thus giving four experimental conditions: N diet and treatment, N diet and placebo, low-CHO diet and treatment and low-CHO diet and placebo. Treatments were assigned using a randomised protocol. Arterialised venous blood samples were taken for the determination of acid-base status and metabolite concentrations at rest prior to exercise and at intervals for 30 min following exhaustion. Consumption of the low-CHO diet induced a mild metabolic acidosis which was reversed by the ingestion of NaHCO(3). Blood pH, bicarbonate (HCO-(3)) and base excess (BE) were higher following NaHCO(3) ingestion after the normal diet than all of the other experimental conditions (P <0.01). Exercise time following the low-CHO diet was less than on the normal diet conditions (P <0.05): bicarbonate ingestion had no effect on exercise time on either of the diet conditions. Post-exercise blood pH, HCO-(3); and BE were higher following the ingestion of NaHCO(3) irrespective of the pre-exercise diet (P <0.05). Blood lactate concentration was higher 2 min after exercise following the N diet with NaHCO(3) when compared to the low-CHO diets with either NaHCO(3) or placebo (P <0.05). Plasma ammonia accumulation was not significantly different between experimental conditions. These data confirm previous data showing that the ingestion of a low-CHO diet reduces the capacity to perform high-intensity exercise, but it appears that the metabolic acidosis induced by the low-CHO diet is not the cause of the reduced exercise capacity observed during high-intensity exercise under these conditions.

Acid-Base Equilibrium↗
PubMed1996

Changes in the profile of liver enzymes in newborn calves induced by experimental, subclinical acidosis in pregnant cows and osmotic diarrhoea.

Experimental, subclinical acidosis was induced by oral administration of sacharose during the last 2 months of pregnancy in 15 cows. Seven cows and their newborn calves were used as a control group. The liver enzyme activities in the serum and the blood acid-base status were determined in the 15 calves from the cows in the experimental group. Mannitol was administered orally to 8 calves from the experimental group to induce osmotic diarrhoea. It was concluded that subclinical acidosis in pregnant cows alters the biochemical liver profile of their newborn calves, affecting the aspartate aminotransferase, alanine transaminase, beta glucuronidase, glutamate dehydrogenase and bilirubin activities in the serum, which are associated with oedematous changes to the hepatocytes. Diarrhoea was accompanied by an increase in the alkaline phosphatase and gammaglutamyl transferase activities and a decrease in the total protein concentration in the serum. These changes were apparently related to the numerous necrotic foci in the liver and the proliferation of the Kuppfer cells. It would appear from these results that the liver damage in the newborn calves was associated with the subclinical, metabolic acidosis in their dams and that osmotic diarrhoea occurring in the neonatal period additionally impaired the liver function.

Acid-Base Equilibrium↗
PubMed1991

Combined inhibitory actions of acidosis and phosphate on maximum force production in rat skinned cardiac muscle.

Possible interactions between the effects of pH and phosphate (Pi) on the maximum force development of cardiac myofibrils were investigated in rat skinned trabeculae in solutions of different pH (7.4-6.2) and [Pi] (where [] denote concentration). At pH 7.0 there was an inverse linear relationship between force and log [Pi] over the [Pi] range 0.2-20 mM; its slope (-0.46/decade) was twice that found previously for skeletal muscle [21]. Acidosis depressed force substantially, but the relative change of force was unaffected by Pi addition (0, 5, 20 mM); there was no evidence for the synergism between acidosis and Pi that would be expected if some of the inhibition by acidosis was due to protonation of Pi to the putative inhibitory form, H2PO4-. It was taken into account that even without Pi addition, there was enough Pi inside the muscle from various sources to produce significant changes in [H2PO4-] as the pH was varied. The results suggest that H+ and Pi inhibit maximum force development of cardiac myofibrils independently, by different mechanisms. From this it is argued that H+ and Pi may be released at different steps in the crossbridges cycle. In the myocardium Pi and H+ probably exert tonic inhibitory influences on cardiac myofibrils under all conditions.

Acidosis↗
PubMed1993

Can insulin administration cause an acute metabolic acidosis in vivo? An experimental study in dogs.

Insulin is the cornerstone of therapy for diabetic ketoacidosis because it causes the rate of ketoacid production to fall; this action takes several hours to occur. Insulin also causes H+ to be transported from the intracellular fluid to the extracellular fluid in vitro. The purpose of this study was to determine if insulin led to the acute export of H+ from the intracellular fluid in vivo. If so, we wished to determine if this also occurred during chronic metabolic acidosis, to quantitate the magnitude of the H+ shift, and to evaluate the mechanisms involved. The administration of low- or high-dose insulin to normal dogs and high-dose insulin to dogs with chronic metabolic acidosis caused the concentration of bicarbonate in plasma to decline by close to 3 mmol/l. The PCO2 fell by close to 15% in all three groups of dogs, so one component of the fall was due to hyperventilation. As the pH of blood did not change, a primary metabolic acidosis also occurred. The fall in bicarbonataemia was not due to net accumulation of organic acids or to a loss of bicarbonate or organic anions in the urine. Taken together, insulin, when given at doses used to treat diabetic ketoacidosis, might induce a significantly greater degree of acidaemia in the extracellular fluid acutely after it is given.

Acidosis↗
PubMed1982

D-lactic acidosis in two patients with short bowel syndrome: bacteriological analyses of the fecal flora.

Two cases of D-lactic acidosis associated with short bowel syndrome are described. The administration of kanamycin to the patients showed a decrease in D-lactate in blood and urine in parallel with disappearance of metabolic acidosis. Bacteriological analyses of the fecal flora showed an increase in Lactobacillus buchneri in the first patient and Lactobacillus fermenti IVa in the second; both bacteria were sensitive to kanamycin. Quantification of in vitro production of D-lactate by each species of bacteria isolated from the feces revealed that Lactobacillus produced more D-lactate than other species of bacteria. These observations indicate that Lactobacillus may play an important role in the induction of D-lactic acidosis in patients with short bowel syndrome.

Acidosis↗
PubMed1985

Influence of respiratory acidosis or alkalosis on pressor responses mediated by alpha 1- and alpha 2-adrenoceptors in pithed normotensive rats.

The effect of respiratory acidosis and alkalosis on the vasoconstriction to alpha 1- and alpha 2-adrenoceptor stimulation was studied in pithed normotensive rats. The selective alpha 1-adrenoceptor agonists (-)amidephrine, cirazoline, (+/-)erythro methoxamine, (-)phenylephrine, Sgd 101/75 and St 587 were used, as well as the selective alpha 2-adrenoceptor agonists B-HT 920, B-HT 933, DP-6,7-ADTN, M-7 and UK 14,304. The non-selective alpha-adrenoceptor agonists xylazine, noradrenaline and adrenaline were included as well. The latter two were also studied under selective doses of the antagonists rauwolscine and prazosin, thus yielding the respective alpha 1- and alpha 2-adrenoceptor components of the vasoconstriction to these agonists. The effect of acid-base balance disturbances on presynaptically released noradrenaline elicited by electrical stimulation of preganglionic nerves was studied as well. Dose response curves for the agonists were generated under various conditions of ventilation, yielding either alkalotic, normal or acidotic values of arterial blood pH. Pressor responses to all agonists were maximally affected by changes in acid-base status at the low doses of the agonists. Acidosis was found to inhibit increases in diastolic pressure mediated by the alpha 1-as well as the alpha 2-adrenoceptor agonists studied, although not to the same extent. Alkalosis exerted either an obvious potentiation or did not significantly influence alpha 1-adrenoceptor mediated pressor responses. On the basis of acid-base sensitivity the following groups of agonists were distinguished: Cirazoline, phenylephrine, methoxyamine, electrically released noradrenaline from presynaptic sites, of which pressor responses are obviously potentiated and attenuated by alkalosis and acidosis, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)

Acid-Base Equilibrium↗
PubMed1986

Intra- and inter-nephron heterogeneity of gluconeogenesis in the rat: effects of chronic metabolic acidosis and potassium depletion.

The intra- and inter-nephron heterogeneity of renal gluconeogenesis within rat proximal tubules and the effects of chronic metabolic acidosis and chronic potassium(K)-depletion were studied using isolated proximal tubules of rats by directly measuring glucose synthesized. The gluconeogenic activity from pyruvate and glutamine in control rats was almost limited to within the early proximal tubule (S1: 45.4 +/- 5.7 pmol/mm/60 min from pyruvate; 58.0 +/- 6.0 from glutamine). Very low, but detectable gluconeogenesis was observed in the middle portion of the proximal tubule (S2: 9.9 +/- 2.2 from pyruvate; 4.8 +/- 1.1 from glutamine). The rate of glucose production in the terminal proximal tubule (S3) was negligible. Furthermore, gluconeogenesis from glutamine of superficial (SF) nephrons was significantly higher than that of juxtamedullary (JM) ones, whereas no difference was seen in gluconeogenesis from pyruvate. In acidotic and K-depleted rats, significant increase could be seen in S1 and S2, but the increase in S3 was not significant. By the serial determination in acidosis, the glucose production from both substrates was found to be the highest at the second 1 mm segment from the glomerulus, and it decreased downward along the proximal tubule. In acidosis, glucose production from both substrates in SF nephrons and that from glutamine in JM ones were elevated significantly compared with the control, but that from pyruvate in JM nephrons did not change. These results suggest that S1 of the SF nephron plays the most important role in gluconeogenesis in the control, whereas S1 of the JM nephron and S2 contribute to gluconeogenesis in acidotic and/or possibly K-depleted rats.

Acidosis↗
PubMed1985

Effect of chronic metabolic acidosis on ammonia production from L-glutamine in microdissected rat nephron segments.

To evaluate the role of each nephron segment in renal ammoniagenesis, distribution of renal ammoniagenic activity along the nephron in control and acidotic rats was examined. We used our original aerobic incubation system and ammonia produced from glutamine in 7 defined segments of microdissected nephron was measured using the enzymatic cycling method. When ammonia production in the control was compared in each nephron segment, the highest specific activity of ammoniagenesis per mm tubular length and that per microgram protein were observed in the proximal straight tubule (PST) and the thick ascending limb of Henle's loop, respectively. Chronic metabolic acidosis increased ammonia production per mm tubular length markedly in the proximal convoluted tubule (PCT) (+171%), moderately in the medullary collecting tubule (+123%) and PST (+77%), and slightly in the distal convoluted tubule (+52%), revealing that the highest activity of ammoniagenesis was located in PCT and PST in acidosis. These data indicate that proximal tubules have major roles in renal ammoniagenesis both in the control and in acidosis. From the early observation of glutaminase I isoenzyme distribution along the nephron, our data suggest that not only phosphate-dependent glutaminase but also phosphate-independent glutaminase may have important roles in renal ammoniagenesis.

Acidosis↗
PubMedDate not supplied

Transient pre-ischemic acidosis protects the isolated rabbit heart subjected to 30 minutes, but not 60 minutes, of global ischemia.

Adenosine released during brief episodes of ischemia, due to the breakdown of ATP, is thought to be an endogenous mediator of ischemic preconditioning. In this study we sought to determine whether protons, also released from ATP during ischemia, may protect the heart from sustained ischemic insult. Experiments were performed in isolated Langendorff-perfused rabbit hearts. Proton release was simulated by a brief transient episode of preischemic acidosis. Before ischemia all hearts underwent 15 min of preischemic perfusion. Control hearts received 15 min perfusion with normal Krebs-Henseleit buffer (KHB; pH 7.39) while the short-term acidosis (STA) group received 5 min of perfusion with normal KHB followed by 5 min of perfusion with acidic buffer (pH 5.97), and then 5 min of perfusion with normal KHB. Both control and STA groups then underwent 30 min of global ischemia. A second pair of control and STA groups were subjected to 60 min of global ischemia. After global ischemia all hearts received 60 min of reperfusion. The time course of functional recovery after 30 min of ischemia was accelerated in the STA group (i.e., developed pressure in the control and STA groups at 15 min into reperfusion averaged 57 +/- 9 and 74 +/- 3 mmHg, respectively; p < 0.05), and a strong trend towards lower release of creatine kinase after 30 min of global ischemia was observed in the STA group (43 +/- 7 U/g dry tissue in the STA group vs. 76 +/- 15 U/g dry tissue in the control group). However, after 60 min of global ischemia no differences in cardiac function at reperfusion were observed between control and STA groups. Our results indicate that in the isolated rabbit heart, brief acidosis affords protection against 30 min but not against 60 min of global ischemia.

Acidosis↗
PubMed1990

Renal tubular acidosis.

The term renal tubular acidosis (RTA) is applied to a group of transport defects in the reabsorption of bicarbonate (HCO3-), the excretion of hydrogen ions, or both. On clinical and pathophysiological grounds, RTA can be separated into three main types: distal RTA (type 1), proximal RTA (type 2) and hyperkalaemic RTA (type 4). Some patients present combined types of proximal and distal RTA or of hyperkalaemic and distal RTA. Diagnosis of RTA should be suspected when a patient presents a normal plasma anion gap, and hyperchloraemic metabolic acidosis. A normal plasma anion gap (Na(+)-[Cl- + HCO3-] = 8-16 mEq/l) reflects loss of HCO3- from the extracellular fluid via the gastro-intestinal tract or the kidney, dilution of extracellular buffer or administration of hydrochloric acid (HCl) or its precursors. Distinction of RTA from other disorders is greatly facilitated by the study of the urine anion gap (Na+ + K+ - Cl-). This index estimates the urinary concentration of ammonium in a patient with hyperchloraemic metabolic acidosis. A negative urine anion gap (Cl- much greater than Na+ + K+) suggests the presence of gastro-intestinal or renal loss of HCO3-, while a positive urine anion gap (Cl- less than Na+ + K+) is indicative of a distal acidification defect. Determination of plasma potassium, of urine pH at low plasma HCO3- concentration, and of urine PCO2 and fractional excretion of HCO3- at normal plasma HCO3- concentration permits the differentiation between the various types of RTA.

Acidosis, Renal Tubular↗
PubMed1992

Transient neonatal distal renal tubular acidosis with secondary hyperparathyroidism.

We describe a neonate with distal renal tubular acidosis with secondary hyperparathyroidism manifesting as hyperchloraemia, hypercalcaemia, elevated serum parathyroid hormone (PTH) and life-threatening metabolic acidosis. He exhibited general weakness, tachypnoea, dry skin and weight loss. Urinary excretion of titratable acid and ammonium was decreased. Daily alkali (2.5 mEq/kg body weight) was required to maintain a normal plasma bicarbonate (HCO3-). With alkali therapy, the fractional excretion of HCO3- was below 5%. Serum calcium and PTH were restored to normal promptly on initiation of alkali therapy. After 5 months of alkali therapy, normal growth and urine acidifying ability were restored and alkali therapy was discontinued. The acidification defect in this patient was transient. We consider this patient to be consistent with Lightwood's syndrome of "transient infantile renal tubular acidosis".

Acidosis, Renal Tubular↗
PubMed1991

The syndrome of renal tubular acidosis and nerve deafness. Discordant manifestations in dizygotic twin brothers.

The syndrome of renal tubular acidosis (RTA) and nerve deafness is a distinct nosological entity that is inherited as an autosomal recessive trait. We studied a pair of dizygotic twin brothers both with nerve deafness but only one with RTA. Distal RTA was diagnosed in twin A because of inappropriately high urinary pH (6.9) and low net acid excretion (40.0 muEq/min per 1.73 m2) in the presence of hyperchloraemic metablic acidosis, and fractional bicarbonate excretion of 1.6% at a normal serum bicarbonate concentration. The urine minus blood PCO2 differences (U-B PCO2) during a neutral sodium phosphate load and in alkaline urine induced by bicarbonate supplementation were: 11 and 0 mm Hg, respectively. Twin A developed nephrocalcinosis and, after a 9.5-year follow-up period, was 5.3 cm taller than his brother. Twin B remained asymptomatic. Periodic determinations of blood pH and serum bicarbonate were normal and urine pH decreased to 4.6 in the face of ammonium chloride-induced metabolic acidosis. The U-B PCO2 assessed in alkaline urine was 33.5 mm Hg. Audiograms demonstrated bilateral nerve deafness in both brothers. The presence of deafness without RTA has not been previously reported in this syndrome. This report also shows that a primary distal acidification defect is responsible for the RTA observed in this syndrome.

Acidosis, Renal Tubular↗
PubMed1991

Distal renal tubular acidosis: the value of urinary pH, PCO2 and NH4+ measurements.

Distal renal tubular acidosis (dRTA) is not a single disease. The experimental forms of the syndrome are unsatisfactory as models of the naturally occurring disease, not least because they are seldom complicated by nephrocalcinosis, which is present in the majority of patients with spontaneous disease and contributes to the renal tubular defects found in the syndrome. Impairment of minimal urine pH, reduced urine carbon dioxide tension (PCO2) during passage of alkaline urine, and reduced urinary ammonium (NH4+) excretion, have all been advocated as essential criteria for the diagnosis of dRTA. Minimal urine pH, measured during metabolic acidosis, sulphate infusion, or after oral frusemide, is the yardstick against which other criteria should be assessed. A reduced urinary PCO2 is commonly found in dRTA but is not specific for the syndrome and may be accounted for by tubular defects other than those involving reduced distal hydrogen ion secretion. NH4+ excretion is reduced in most patients with renal acidosis whatever the nature of the underlying renal disease; this function is closely related to nephron mass, and is not specifically impaired in renal tubular disease.

Acidosis, Renal Tubular↗
PubMed1986

Severe osteomalacia associated with renal tubular acidosis in Crohn's disease.

Severe renal tubular acidosis associated with massive osteomalacia is described in a patient with Crohn's disease. To our knowledge this association has not been previously recognized. The possible role of renal tubular acidosis in this patient's osteomalacia is discussed and the factors that could be involved in renal tubular acidosis in the context of Crohn's disease are analyzed.

Acidosis, Renal Tubular↗
PubMed1992

Plasma ionized calcium and blood lactate concentrations are inversely associated in human lactic acidosis.

Plasma ionized calcium [Ca++] concentrations are decreased in patients having lactic acidosis. To further investigate this observation, we prospectively studied nine critically ill patients who had lactic acidosis and measured arterial pH, PCO2, [Ca++], lactate, and albumin concentrations. We found a strong association between decreased [Ca++] and increased plasma lactate concentrations (r2 = 0.78, p less than or equal to 0.001). This unexpected association--[Ca++] usually increases with increasing acidosis--might be clinically important and the mechanism deserves further investigation.

Acidosis, Lactic↗
PubMed1982

Acquired distal renal tubular acidosis in man.

Distal renal tubular acidosis (dRTA) may complicate renal transplantation, liver cirrhosis, and obstructive uropathy. Indeed, its occurrence may be an early clue to an episode of rejection of the graft or to obstructive uropathy. The mechanism in most patients with dRTA is impaired distal secretion of protons. In some patients, however, back leak of protons from tubular lumen to blood may abolish distal tubular ability to maintain urine to blood proton gradients. In patients with obstructive uropathy the spectrum of tubular acidosis is widened by the occurrence of additional defects in tubular secretion of potassium and impairment of hydrogen ion secretion secondary to hypoaldosteronism. Hyperkalemia is also seen in "voltage dependent" states such as following the administration of lithium and amiloride. Hyperkalemia per se is conducive to acidosis by a combination of extrarenal and several intrarenal mechanisms.

Acidosis, Renal Tubular↗