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PubMed1985

Long-term monitoring of D-lactic acidosis in a child.

A case of D-lactic acidosis in a 2 1/2-year-old child followed for 11 months is reported. The infant had previously undergone extensive small intestinal resection for midgut volvulus. Diagnosis was confirmed by measurement of plasma D-lactate. Metabolic acidosis, increased anion gap, ataxia, and lethargy in patients with small intestinal resection warrant investigation for D-lactic acidosis. The presumed etiology is absorption of D-lactic acid produced by bacterial fermentation of carbohydrate in the colon. Antibiotic treatment resulted in prompt resolution of symptoms in this case. Prospective and prolonged monitoring of acidosis in patients with small bowel resection is encouraged.

Acidosis↗
PubMed1977

Lactic acidosis complicating diabetic ketosis in a patient with hyperthyroidism.

The present report describes a patient with insulin-dependent diabetes who developed simultaneously lactic acidosis and ketoacidosis following insulin deprivation. Administration of insulin at low doses rapidly corrected both ketosis and lactic acidosis. There had been neither circulatory collapse, nor phenformin intake, and hepatic function was normal. The development of lactic acidosis in this case was possibly precipitated by hyperthyroidism. A review of the literature indicates that lactic acidosis is a very rare complication of diabetic ketosis per se.

Acidosis↗
PubMedDate not supplied

Blood acid-base equilibrium in experimental acidosis of the rumen in sheep.

Blood acid-base equilibrium in experimental acidosis of the rumen in sheep. Acta Physiol. Pol., 1979, 30 (4): 543--551. Experimental acidosis of the rumen was induced in sheep infusing into it through a fistula a solution of saccharose and solutions of different volatile fatty acids and lactic acid. Arterial-blood acid-base equilibrium indices were determined by the Astrup micromethod with an Acid-Base-Cart ABC-1 unit. It was found that during saccharose-acidosis partly compensated metabolic acidosis develops and that acid-base equilibrium disturbances are caused by all volatile fatty acids and lactic acid. When they are infused in equimolar amounts into the rumen the strongest and earliest disturbances in that equilibrium are caused by acetic acid, followed by butyric, lactic and propionic acids.

Acidosis↗
PubMed1984

Na+-H+ exchange in isolated renal brush-border membrane vesicles in response to metabolic acidosis. Kinetic effects.

Chronic metabolic acidosis increased the Na+-H+ exchange activity in isolated renal brush-border membrane vesicles. Treatment altered the initial rate of Na+ uptake by increasing Vm (acidotic, 15.3 +/- 0.7 nmol of Na+ X mg-1 X 2 s-1; normal, 11.3 +/- 0.9 nmol of Na+ X mg-1 X 2 s-1), and not the apparent affinity KNa+ (acidotic, 10.2 +/- 0.5 mM; normal 10.2 +/- 0.6 mM). Metabolic acidosis resulted in the proportional increase in 1 mM Na+ uptake at every intravesicular pH measured. A positive cooperative effect on Na+ uptake was found with increased intravesicular acidity in vesicles from both normal and acidotic rats. When the data were analyzed by the Hill equation, it was found that metabolic acidosis did not change the n (acidotic, 1.33 +/- 0.13; normal, 1.43 +/- 0.07) or the K'H+ (acidotic, 0.27 +/- 0.05 microM; normal, 0.28 +/- 0.06 microM), but increased the apparent Vm (acidotic, 1.10 +/- 0.08 nmol of Na+ X mg-1 X 2 s-1; normal, 0.81 +/- 0.07 nmol of Na+ X mg-1 X 2 s-1). The uptake of Na+ in exchange for H+ in membrane vesicles from normal and acidotic animals was not influenced by membrane potential. We conclude that metabolic acidosis leads to either an increase in the number of functioning exchangers or an increase in the turnover rate of the limiting step in the exchange.

Acidosis↗
PubMed1983

Renal tubular acidosis. A new look at treatment of musculoskeletal and renal disease.

The clinical and laboratory manifestations, roentgenographic findings, and treatment of 48 patients with renal tubular acidosis who were examined at the Mayo Clinic during a 10-year period were reviewed. The initial clinical presentations of the 48 patients in the series included rheumatic complaints in 25 and recurrent nephrolithiasis in 23. Of the 23 patients who presented with nephrolithiasis, 8 also had musculoskeletal symptoms. Thirty-three of the 48 patients had careful follow-up of a total of 68 musculoskeletal complaints. Forty of these symptoms (59%) diminished after treatment of the renal tubular acidosis with orally administered alkali. Associated connective tissue diseases were present in 12 patients. Thirty-four patients had roentgenographic evidence of renal calculi. Of this group, 19 were followed up with sequential roentgenographic studies of the kidneys for more than 1 year during therapy. Of 15 patients treated orally with alkali, 13 had metabolically inactive renal stone disease. Three of the patients treated orally with phosphorus supplements had persistent metabolically active renal stone disease. Patients with renal tubular acidosis often present with musculoskeletal manifestations and renal lithiasis, both of which frequently subside with the treatment of the renal tubular acidosis.

Acidosis, Renal Tubular↗
PubMed1980

Effect of acute metabolic acidosis on the renin-aldosterone system. Mechanism of increases in plasma aldosterone in dogs infused with lactic acid.

Recent observations suggest that PA increases during acute metabolic acidosis. The pathophysiological mechanism(s) involved remains undefined. In the present study, anesthetized mongrel dogs were infused with lactic acid (10 mEq/kg body weight) for 3 hr. During acidosis there was no change in plasma potassium concentration, a tendency for an incrase in PRA, and significant increases in PC (as a marker for ACTH secretion) and PA. Other dogs were infused with lactic acid after prior treatment with dexamethasone and propranolol or with dexamethasone alone. Under these conditions, the development of acidosis was not associated with changes in PC, plasma potassium, PRA, or PA, suggesting that the stimulatory effect of acidosis on PA is not a direct one but is mediated by concomitant increases in ACTH and/or PRA.

Acidosis↗
PubMed1984

Glycolate causes the acidosis in ethylene glycol poisoning and is effectively removed by hemodialysis.

Six male patients with severe ethylene glycol poisoning were studied with respect to the origin of the metabolic acidosis. The plasma concentrations of ethylene glycol were 4-41 mmol/l and treatment included alkali, ethanol and hemodialysis. Plasma analysis by isotachophoresis and whole blood lactate determinations showed that glycolate (17.0-29.3 mmol/l), lactate (1.4-6.2 mmol/l) and beta-hydroxybutyrate (less than or equal to 1.8 mmol/l) were present in elevated concentrations contributing to the acidosis. Oxalate (less than or equal to 0.33 mmol/l), glyoxylate (less than 0.2 mmol/l) and formate (less than 0.4 mmol/l) concentrations were negligible and did not contribute to any significant degree to the acidosis. The elevated plasma glycolate concentration was highly correlated to the anion gap (r = 0.923) and the glycolate made up for 96.1% (n = 6, range 84.7-108.8) of the increased anion gap. We conclude that glycolate accumulation is the main reason for the metabolic acidosis in ethylene glycol poisoning. The mean dialysator (1.6 m2) clearances of glycolate at a blood flow of 200 ml/min in two patients were 137 ml/min (n = 9, SD +/- 8, range 125-149) and 144 ml/min (n = 11, SD +/- 8, range 133-158). By applying first order kinetics during hemodialysis a volume of distribution of glycolate of 0.55 l/kg was found, assuming that the dialysator clearance equals the total body clearance of glycolate. Thus glycolate, the probable main metabolite of ethylene glycol, is efficiently removed by hemodialysis.

Acidosis↗
PubMed1983

Lactic acidosis in a patient with acute leukemia.

Lactic acidosis is a rare but potentially fatal complication of acute leukemia. The terminal phase of acute leukemia in a 22-year-old woman, heralded by lactic acidosis, is described in order to focus attention on the occurrence of this metabolic disturbance in the absence of overt manifestations of acute leukemia. As reported in other cases, the lactic acidosis in our patient responded poorly to bicarbonate therapy but dramatically to antileukemic chemotherapy. The pathogenesis of the lactic acidosis is unclear but it may be the result of an undefined 'paraneoplastic' metabolic disturbance induced by the leukemic cells.

Acidosis↗
PubMed1984

Neonatal acidosis and method of delivery.

Seven hundred and four women who had a forceps termination (177 elective, 293 indicated low, and 234 indicated midforceps) of labor over 24 months were compared with 303 spontaneous and 111 cesarean deliveries over the same time period. There was no significant difference between indicated low or midforceps either for fetal distress or arrest of descent with regard to fetal acidosis (pH less than 7.20), one- or five-minute Apgar scores less than 7, fetal trauma, or neurologic deficit at discharge. Fourteen percent of indicated forceps for arrest of descent had neonatal acidosis, versus 8% of cesarean sections for cephalopelvic disproportion (P = NS), and 23% of indicated forceps for fetal distress had acidosis, versus 33% of cesarean sections (P = not significant). There was no significant difference either in the incidence of acidosis or in low Apgar scores in neonates delivered by elective low forceps compared with those born by spontaneous vaginal delivery. The only significant differences in midforceps versus low forceps were between maternal pre- and postdelivery hematocrits (P less than .0001) and vaginal lacerations (P less than .0001). The authors' data support the continued usage of indicated low and selected midforceps operations.

Acidosis↗
PubMed1983

[Methemoglobinemia and acidosis during the first week of life].

Recently attention has been called on the possible role of acidosis in the increased methemoglobin formation in the erythrocyte of newborn infant. In the present paper the relations between acidosis and methemoglobin content in the red cells of newborns has been investigated. No significant differences between the percent of methemoglobin in the normal newborns and percent of methemoglobin in the newborns with acidosis has been found. In addition, no correlations between the base excess and percent of methemoglobin has been observed. On the contrary, two newborns with low glucose-6-phosphate dehydrogenase activity demonstrated a significantly increased methemoglobin content in their red cells. The results of our study do not confirm a key role of acidosis in the mechanism of methemoglobin formation in the neonate. It is likely than impairment of red cell metabolism should be the main factor in the formation of methemoglobin in the first days of life.

Acidosis↗
PubMed1981

[Liver function in cattle in experimental rumen acidosis].

The investigations were performed on 6 Friesian-Holstein heifers, weighing 410-504 kg, in which acid indigestion was induced by intraruminal administration of saccharose in a dose of 12 g/kg body weight. The animals were observed for 9 days after the treatment. Functional state of the liver was evaluated on the basis of bromosulphthalein clearance, total bilirubin level and aspartate amino-transferase (AspAT) activity in serum, concentration of blood glucose, total serum protein and protein fractions. Within the first 24 hours, all heifers developed acute symptoms of rumen acidosis which persisted for 3 days after saccharose administration. Afterwards, a phase of gradual spontaneous recovery was observed. In the course of rumen acidosis a reduction in bromosulphthalein clearance, an increase in bilirubin level and AspAT activity, a decrease and then an increase in glucose concentration and a reduction in albumin content and, as a consequence, in albumin/globulin ratio were found. The results indicate that experimental rumen acidosis produced disturbances in excretory and metabolic functions of the liver in the examined heifers. Changes in biochemical parameters were preceded by an increase in AspAT activity and were most remarkable between 48 and 144 hours after saccharose administration. Liver dysfunction was of a various degree in individual animals and recovered within a relatively short period following the disappearance of rumen acidosis symptoms.

Acidosis↗
PubMed1981

[Acute acidosis in a bovine].

A case of acute acidosis due to over-ingestion of maizemeal is reported. The cow was in sternal recumbancy, unable to rise and showed signs of severe dehydration, metabolic acidosis and rumen stasis. Examination of rumen contents revealed changes consistent with those of lactic acidosis. Treatment included correction of the metabolic acidosis, restoration of intravascular volume, manipulation of rumen contents including rumen lavage and other supportive treatment. Some pathophysiological aspects and the need for a systematic and vigorous treatment regime are discussed.

Acidosis↗
PubMed1978

Relationship of metabolic acidosis to urinary sodium excretion in the newborn infant.

The relationship between birth weight, postnatal age and acidosis-induced urinary sodium excretion was studied in 43 one-week-old newborn infants with birth weights of 1000-4300 g and gestational age of 28-41 weeks; and in 13 premature infants with birth weights of 1000-1970 g (mean 1620 g) and gestational age of 29-35 weeks (mean, 31.4 weeks) during the first six weeks of life. Developmental changes were found in acidosis-induced urinary sodium excretion. Newborns with higher birth weight and postnatal age excreted significantly more sodium in response to acidosis than their lighter and younger matches. It is suggested that the degree of acidosis must be taken into account when estimating the sodium requirement of newborn infants different in birth weight and postnatal age.

Acidosis↗
PubMed1995

Role of metabolic acidosis on cardiac mechanical performance during severe acute hypoxia and reoxygenation is small and transient.

OBJECTIVE: The aim was to determine whether the metabolic acidosis that develops during severe acute myocardial hypoxia improves or impairs the recovery of cardiac mechanical function during reoxygenation. METHODS: Isolated rat hearts performed external work against a model of the rat systemic vascular impedance. Four groups of 10 hearts were used for mechanical studies. In these experiments, the hearts were subjected to normoxic ventilation for 15 min, hypoxic ventilation for 20 min, and reoxygenation for 60 min. The perfusate pH was either allowed to drift downward due to metabolic acidosis, or it was corrected to 7.4 as hypoxia or reoxygenation began. Mechanical performance was assessed by measuring heart rate and model "aortic" pressure and flow and by computing left ventricular mean, pulsatile, and total hydraulic power output and stroke work. A further four groups of 10 hearts were used for biochemical studies. In these experiments, myocardial high energy phosphates and calcium content were measured at the end of the period of hypoxia. RESULTS: When no attempt was made to regulate the perfusate pH, it drifted downward from 7.40(SEM 0.01) to 7.33(0.01) during hypoxia and then to 7.25(0.02) during reoxygenation. All mechanical variables measured and computed were severely depressed by hypoxia, whether the pH was regulated or not. Left ventricular total hydraulic hydraulic power output decreased to less than 10% of the control value in all experiment groups and recovered to 86.7-91.2% of the control value after 60 min of reoxygenation. Mechanical recovery was most rapid when the correction of acidosis was delayed until reoxygenation was begun. After 5 min of reoxygenation, it had recovered to 65.5% of the control value compared with a 37.0% recovery when the pH was allowed to drift and 34.9% when the pH was corrected to 7.4 during hypoxia. However, the differences in power output became non-significant after 10 min of reoxygenation. Myocardial creatine phosphate and adenosine triphosphate concentrations were decreased by hypoxia whether the pH was corrected (63.0% and 26.9% relative to the control), or not (68.9% and 35.0% relative to the control) (not statistically significant), but total cell calcium was not affected. CONCLUSIONS: In the isolated rat heart, correction of the moderate metabolic acidosis that developed during severe acute myocardial hypoxia improved the rate of mechanical recovery, but the effect was small and not sustained.

Acidosis↗
PubMed1995

Hypercapnic acidosis and dimethyl amiloride reduce reperfusion induced cell death in ischaemic ventricular myocardium.

OBJECTIVE: The aim was to investigate the effects of slowing the recovery of ischaemia induced intracellular acidosis with hypercapnic acidosis or dimethyl amiloride (DMA) on the extent of reperfusion induced cell death. METHODS: Isolated arterially perfused rabbit papillary muscles and septa were suspended in a controlled atmosphere and perfused with a modified Tyrode solution containing erythrocytes and trypan blue (500 microM). Ischaemia was produced by arrest of perfusion and withdrawal of atmospheric O2. Extracellular pH of the muscle during reperfusion was controlled by adjusting the pH of the perfusate (pH 6.6 or pH 7.6 with and without DMA 20 microM) and changing the PCO2 of the chamber atmosphere. After 30 min of reperfusion following 30 min (group A) or 60 min (group B) of ischaemia, papillary muscles were fixed with paraformaldehyde. Cell death was assessed by trypan blue staining of nuclei in histological sections of the papillary muscles. RESULTS: The magnitude of cell death was greatest after reperfusion with pH 7.6 as measured by the percentage of nuclei staining with trypan blue (15.1% in group A; 41.8% in group B). By contrast, reperfusion at pH 6.6 reduced cell killing (group A, 3.6%; group B, 7.2%). Reperfusion at pH 7.6 with DMA (20 microM) also reduced trypan blue uptake (group A, 2.8%; group B, 3.8%). Despite the attenuation of cell death afforded by acidosis or Na+/H+ exchange inhibition, significant swelling of the extracellular space and microvascular injury was noted. CONCLUSIONS: Hypercapnic acidosis and Na+/H+ exchange inhibition during reperfusion attenuate lethal reperfusion injury to ventricular myocardium and extend to the intact myocardium the concept of the "pH paradox" in which recovery of intracellular pH after reperfusion is a precipitating factor in lethal cell injury.

Acidosis↗
PubMed1994

[Clinical spectrum of distal renal tubular acidosis and its study with bicarbonate loading].

Authors attempted to review the clinical spectrum of distal renal tubular acidosis on the basis of analysing the records of 11 patients. Distal renal tubular acidosis was associated with chronic renal failure of different severity and with tubulointerstitial diseases in the two-third of patients in whom histologic studies were also performed. The disorders caused in certain cases hypokalemia and hyperkalemia in the others, the concentrating insufficiency was characteristic leading in exceptional cases to nephrogenic diabetes insipidus and the clinical picture was accompanied also by osteomalacia. Authors describe their own method of bicarbonate loading, obtaining by its use very high values of 78.65 +/- 11.28 (p < 0.005) mmHg of urine minus blood pCO2 in 6 healthy subjects. On the other hand, in 6 distal renal tubular acidosis patients no such difference in the pCO2 values could be found. The knowledge of the clinical spectrum of the distal renal tubular acidosis may enhance the recognition and treatment of the disorder.

Acidosis, Renal Tubular↗
PubMed1994

Enzymatic and functional evidence for adaptation of the vacuolar H(+)-ATPase in proximal tubule apical membranes from rats with chronic metabolic acidosis.

The present work examined the effects of chronic metabolic acidosis on the vacuolar proton-translocating adenosine triphosphatase (H(+)-ATPase) activity both in rat renal cortical homogenates and in their luminal membranes. Moreover, to assess the effect of acidosis on H+ transport by the apical H(+)-ATPase, we have developed a detergent-dilution procedure, resulting in the formation of sealed vesicles having this enzyme at their external surface. NH4Cl loading for 4 days had no effect on homogenates H(+)-ATPase activity, estimated with either N-ethylmaleimide or bafilomycin A1. In contrast, H(+)-ATPase activities were increased significantly by about 30% in both native apical membranes prepared by Ca2+ aggregation and detergent-treated luminal vesicles from acidotic animal. Kinetic analysis revealed that this stimulation was solely through changes in the Vmax for ATP. In membranes prepared by Mg2+ aggregation, acidosis also caused significant stimulation of the H(+)-ATPase activity. In addition, the initial rate of ATP-induced intravesicular acidification was 25% higher in reoriented H(+)-ATPase vesicles from acidotic rats, whereas passive proton permeability was identical in both groups. Finally, both vesicle enrichments and yields of luminal markers and de-enrichments and yields of intracellular membrane markers were identical in the two groups. These results provide enzymatic and functional evidence suggesting that chronic acidosis induces an adaptative change in the rat brush border H(+)-ATPase.

Acidosis, Renal Tubular↗
PubMed1993

[Stimulation of the alpha-1 adrenergic receptors during simulated reperfusion after myocardial acidosis. The evidence for an arrhythmogenic role of the Na+/H+ exchanger].

Myocardial ischemia is associated with an intracellular acidosis recovering after reperfusion. Alpha 1-adrenergic stimulation (alpha 1) exacerbates ischemic injury and triggers ventricular arrhythmias during the reperfusion phase. We have tested the hypothesis that the arrhythmogenic effect of alpha 1 is due to a cytosolic alkalinization secondary to proteinkinase C (PKC)-dependent activation of the sarcolemmal Na+/H+ exchanger. In addition, the effect of the 2 distinct receptor subtypes, alpha 1A and alpha 1B, has also been evaluated. We used single, enzymatically dissociated, adult rat ventricular myocytes. Cells were loaded with the ester derivative of the Ca2+ probe, indo-1 or with the intracellular pH probe SNARF-1. Fluorescence was monitored simultaneously with contractility and was taken as an index of intracellular [Ca2+] or as pHi value. Cells on a stage of an inverted microscope were superfused with a bicarbonate buffer continuously gassed with 95% O2 and 5% CO2 (pH = 7.37; Ca2+ 1.5 mM) and electrically stimulated at 0.5 Hz, at 25 degrees C. Alpha 1 (phenylephrine 50 microM + nadolol 1 microM) increased twitch amplitude and pHi (delta pHi = 0.05 +/- 0.01; pHi in control = 7.24 +/- 0.06, n = 10; p < 0.05). This effect was abolished by the PKC inhibitor staurosporine (5 nM), by overnight (12-24 hours) exposure to 0.2 microM phorbol esters and by the perfusion with 10 microM ethylisopropylamiloride (EIPA), a Na+/H+ exchange inhibitor. During 15 min of hypercarbic acidosis, achieved by switching to a buffer equilibrated with 85% O2 and 15% CO2 (pH = 7.01), alpha 1 had a more pronounced effect on pHi (delta pHi = 0.11 +/- 0.02; pHi in control = 7.02 +/- 0.04, n = 10; p < 0.05). During the 10 min following the removal of acidosis, alpha 1 induced aftercontractions in 75% (n = 20) versus only 25% (n = 8) of the cells in the absence of phenylephrine (p < 0.05). Superfusion with 10 microM EIPA (n = 6) abolished the occurrence of aftercontractions. Selective alpha 1A-adrenergic receptors stimulation (alpha 1 + 2 microM CEC, which inactivates alpha 1B receptors) further increased them (92%, n = 12) whereas selective alpha 1B-adrenergic receptors stimulation (alpha 1 + 2 microM WB-4101, a alpha 1A receptors antagonist) greatly reduced the occurrence of aftercontractions (11%, n = 18). These results show that the PKC-mediated activation of the Na+/H+ exchanger is the mechanism for the arrhythmias induced by alpha 1 during simulated reperfusion after a period of acidosis.(ABSTRACT TRUNCATED AT 400 WORDS)

Acidosis↗