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PubMed1997

Correction of acidosis in dialysis patients increases branched-chain and total essential amino acid levels in muscle.

Earlier studies have shown increased oxidation of the branched-chain amino acids (BCAA), valine, isoleucine and leucine, in experimental acidosis and low levels of valine in the muscle of acidotic HD patients. Using HPLC, free amino acids in plasma and muscle were studied before and after correction of acidosis in 9 HD patients over 6 months by dialysis with a high bicarbonate solution. The predialysis standard bicarbonate concentration in blood increased from 20.6 +/- 1.3 mmol/l (mean +/- SD) before correction of acidosis to 25.9 +/- 1.8 mmol/l after correction. Correction of acidosis resulted in a significant increase in the i.c. concentrations of valine, isoleucine and leucine by 48%, 28% and 32%, as well as for the sum of BCAA and EAA, from a level lower than controls. The intra- and extracellular gradient increased for several amino acids and for the sum of EAA and BCAA, suggesting an increased influx or reduced efflux of amino acids across the cell membrane. Anthropometric data and the levels of S-albumin and transferrin did not change after correction of acidosis. The increases in the i.c. concentrations of BCAA after correction of acidosis suggest that the catabolism of these amino acids had been reduced. The effects of correction of acidosis on the concentrations of essential amino acids could be beneficial since low concentrations in muscle may reduce protein synthesis.

Acidosis↗

PubMed1998

Participation of P-dependent and P-independent glutaminases in rat kidney ammoniagenesis and their modulation by metabolic acidosis, hippurate and insulin.

The key regulatory enzymes of kidney ammoniagenesis appear to be P-dependent (PDG) and P-independent (PIG) glutaminases. While the participation of PDG has been satisfactorily elucidated, the significance of PIG remains doubtful. Rat kidney cortex slices synthesized ammonia even under basal conditions. Metabolic acidosis, hippurate and insulin stimulated ammonia production. Under basal conditions, PDG activity in kidney homogenate, was twice as high as PIG activity. Metabolic acidosis stimulated ammonia production by the stimulation of both PDG (100%) and PIG (57%) activities. Hippurate stimulated only PIG activity both under basal conditions (90%) and in metabolic acidosis (52%), while it inhibited PDG activity only insignificantly under basal conditions and markedly (53%) in metabolic acidosis. Insulin stimulated both PIG and PDG activities under basal conditions as well as in metabolic acidosis and potentiated the PIG stimulation by hippurate while it potentiated the hippurate inhibition of PDG both under basal conditions and in acidotic rats. In conclusion, both PDG and PIG participate in ammoniagenesis and are stimulated by metabolic acidosis and insulin. Hippurate stimulates PIG, while it inhibits PDG in metabolic acidosis and even after insulin administration. The effect of hippurate appears to be of physiological interest.

Acidosis↗

PubMed1983

The epidemiology of diabetic acidosis: a population-based study.

A 12-month epidemiologic study in 1979 and 1980 of all diabetic acidosis admissions to all acute care hospitals in Rhode Island detected 152 episodes occurring in 137 persons. Eleven per cent of diabetic acidosis admissions presented in coma and the overall death-to-case ratio was 9%. Newly diagnosed diabetes accounted for 20% of these episodes, while persons having multiple episodes during the year accounted for 15% of the admissions. The annual rate of diabetic acidosis was 46 per 10,000 diabetics. Highest rates of diabetic acidosis were found for the elderly, those admitted from nursing homes and those residing in one geographic area of the state. For known diabetics with an admission for acidosis, 87% were on insulin prior to admission and 81% were nonobese. Patients seldom contacted physicians prior to admission. Insulin dose or frequency was often (40%) changed in the two weeks prior to admission. Most of the known diabetic cases of acidosis had emergency admissions for diabetes in the three-year period prior to admission and few had any structured diabetic outpatient education. Infection and noncompliance were the most frequently identified precipitants of diabetic acidosis occurring in known diabetics.

Adolescent↗

PubMed1982

Acidosis and contractility of heart muscle.

The contractility of heart muscle is sensitive to small and physiological changes of extracellular pH. The reduction of contractility associated with an acidosis is determined by the fall of pH in the intracellular fluid. The function of many organelles within the cardiac cell is affected by hydrogen ions. The tension generated by isolated myofibrils at a fixed calcium concentration is reduced at low pH. The dominant mechanism for the reduction of contractility in whole tissue is competitive inhibition of the slow calcium current by hydrogen ions. The reduction of the slow calcium current is similar when the same fall of developed tension is induced by acidosis or by a reduction of extracellular calcium concentration. Measurement of tissue pH with fast-responding extracellular electrodes show that, in myocardial ischaemia, tissue acidosis develops at the same time or only seconds before the onset of contractile failure. Much of the reduced contractility can be accounted for by the severity of the acidosis. Although a mild acidosis can delay or prevent damage to the myocardium from ischaemia or hypoxia, a severe acidosis is not beneficial and may even cause tissue necrosis.

Acidosis↗

PubMed1998

Acidosis activates complement system in vitro.

We investigated the in vitro effect of different forms of acidosis (pH 7.0) on the formation of anaphylatoxins C3a and C5a. Metabolic acidosis due to addition of hydrochloric acid (10 micromol/ml blood) or lactic acid (5.5 micromol/ml) to heparin blood (N=12) caused significant activation of C3a and C5a compared to control (both p=0.002). Respiratory acidosis activated C3a (p=0.007) and C5a (p=0.003) compared to normocapnic controls. Making blood samples with lactic acidosis hypocapnic resulted in a median pH of 7.37. In this respiratory compensated metabolic acidosis, C3a and C5a were not increased. These experiments show that acidosis itself and not lactate trigger for activation of complement components C3 and C5.

Acidosis↗

PubMed1985

Effects of acidosis on rat muscle metabolism and performance during heavy exercise.

The metabolism and performance of a perfused rat hindquarter preparation was examined during heavy exercise in three conditions: control (C), metabolic acidosis (MA, decreased bicarbonate concentration), and respiratory acidosis (RA, increased CO2 tension). A one-pass system was used to perfuse the hindquarters for 30 min at rest and 20 min during tetanic stimulation via the sciatic nerve. The isometric tension generated by the gastrocnemius-plantaris-soleus muscle group was recorded, and biopsies were taken pre- and postperfusion. Initial isometric tensions were similar in all conditions, but the rate of tension decay was largest in acidosis; the 5-min tensions for C, MA, and RA were 1,835 +/- 63, 1,534 +/- 63, and 1,434 +/- 73 g, respectively. O2 uptake in C was greater than in MA and RA (23.4 +/- 1.3 vs. 17.0 +/- 1.4 and 16.5 +/- 2.3 mumol X min-1), paralleling the tension findings. Hindquarter lactate release was greatest in C, least in MA, and intermediate in RA. Acidosis resulted in less muscle glycogen utilization and lactate accumulation than during control. Muscle creatine phosphate utilization and ATP levels were unaffected by acidosis. Acidosis decreased the muscle's ability to generate isometric tension and depressed both aerobic and anaerobic metabolism. During stimulation in this model lactate left the muscle mainly as a function of the production rate, although a low plasma bicarbonate concentration at pH 7.15 depressed muscle lactate release.

Acidosis↗

PubMed1980

Stimulation of ammoniagenesis by acute acidosis: evidence for a urinary inhibitor.

To elucidate the factors mediating the response of renal ammoniagenesis to acute acidosis, the isolated perfused rat kidney was subjected to acute metabolic and respiratory acidosis with either standard collection or drainage of urine back into the perfusate. Midway during a 90-min perfusion with 0.4 mM glutamine and 5 mM glucose, perfusate pH was decreased to 6.8 by addition of HCl or alteration of the PCO2. Metabolic acidosis increased NH3 production, acidified the urine, and increased urinary NH4 excretion. Respiratory acidosis increased NH3 production to a comparable degree without urine acidification and with a minimal increase in NH4 excretion. When respiratory acidosis preceded perfusion at control PCO2 levels, NH3 production was increased but NH4 excretion was lower than control values. If urine drained back into the perfusate, NH3 production was not altered by either metabolic or respiratory acidosis. Accordingly, acute changes in perfusate pH stimulate renal ammoniagenesis by the isolated perfusate pH stimulate renal ammoniagenesis by the isolated perfused kidney independent of changes in urinary pH and NH4 excretion. This response is inhibited by an unidentified factor excreted in the urine.

Acid-Base Equilibrium↗

PubMed1989

Net calcium efflux from live bone during chronic metabolic, but not respiratory, acidosis.

In vivo chronic metabolic acidosis induces bone mineral dissolution. Whether the dissolution is due to alterations in physicochemical factors alone, as in acute metabolic acidosis, or requires participation of bone cells is not clear. The effect of chronic respiratory acidosis on bone has also not been established. To determine the effects of chronic metabolic and respiratory acidosis on net calcium flux from bone, we cultured live and dead neonatal mouse calvariae for 99 h in control medium or in medium acidified (pH approximately equal to 7.1) either by lowering the bicarbonate concentration (Met) or by increasing the PCO2 (Resp). We measured net calcium flux (JCa) over 0-48, 48-96, and 96-99 h. Over the first 48 h, there was greater net calcium efflux from live and dead Met than from both Resp groups. All four acidic groups had greater net calcium efflux than controls. Over the last 51 h of the chronic 99 h culture, there was net calcium efflux only from live Met (JCa = 285 +/- 129 nmol.bone-1.3 h-1) and not from any of the other groups (live control, JCa = -183 +/- 24; live Resp, JCa = -110 +/- 22; dead control, JCa = -256 +/- 12; dead Met, JCa = 11 +/- 78; dead Resp, JCa = -27 +/- 47; each P less than 0.02 vs. live Met). There is net calcium efflux from live cultured neonatal mouse calvariae during chronic metabolic, but not respiratory, acidosis. During chronic acidosis, decreased medium bicarbonate, and not just a fall in pH, is necessary to enhance net calcium efflux from live bone.

Acidosis↗

PubMed1997

Acute haemodynamic effects of sodium bicarbonate administration in respiratory and metabolic acidosis in anaesthetized dogs.

Twenty-seven halothane-anaesthetized, mechanically ventilated adult mongrel dogs were randomly assigned to either respiratory acidosis group [pHa 7.22 (0.03, SD), PaCO2 9.6 (1.1) kPa, base excess -0.5 (1.4) mmol.l-1, n = 9], metabolic acidosis group [pHa 7.20 (0.05), PaCO2 5.5 (0.4) kPa, base excess -11.1 (2.1) mmol.l-1, n = 9], or nonacidosis group [pHa 7.37 (0.07), PaCO2 5.2 (0.4) kPa, base excess -1.1 (1.5) mmol.l-1, n = 9]. Respiratory acidosis and metabolic acidosis were induced by decreasing respiratory rate and continuous infusion of 2 mmol.l-1 hydrochloric acid, respectively. Sodium bicarbonate solution 1 mmol.kg-1 was injected into the right atrium over five seconds when haemodynamic stability was obtained. In all three groups, acute administration of sodium bicarbonate produced transient decreases in mean arterial pressure and RV dP/dtmax, and transient increase in right atrial pressure 30 seconds after injections, but these variables returned to the pre-injection values by the end of the three minutes observation period. Although no significant differences were seen in haemodynamic variables among the three groups at 30 seconds, one and three minutes, maximum reductions in both RV dP/dtmax and PBF in the metabolic acidosis group (260 (143) mmHg.s-1 and 0.38 (0.26) l.min-1) were significantly greater than those in the non-acidosis group (127 (34) mmHg.s-1 and 0.08 (0.09) l.min-1; P < 0.05).

Acidosis↗

PubMed1999

Metabolic acidosis and thiamine deficiency.

We describe a 19-year-old patient who was receiving home parenteral nutrition in whom lactic acidosis developed. A review of her home parenteral nutrition formula revealed the absence of multivitamins, most significantly thiamine. After thiamine administration, the acidosis resolved, and the patient experienced pronounced clinical improvement. Clinicians must be aware that thiamine is essential for normal glucose metabolism and that thiamine deficiency can lead to lactic acidosis. Thiamine deficiency should be included in the differential diagnosis of lactic acidosis. The recent shortage of intravenous multivitamin preparations has led to documented cases of lactic acidosis as a result of thiamine deficiency, and a previous shortage led to several deaths due to lactic acidosis as a consequence of thiamine deficiency. All patients receiving parenteral nutrition must also receive adequate vitamin supplementation.

Acidosis↗

PubMed1990

[Water-electrolyte and acid-base imbalance. VI. Metabolic acidosis].

Metabolic acidosis results from a disequilibrium between production and excretion of acid. Loss of base from the body through the gastrointestinal tract or in the urine or an increase in metabolic acid production are the three major mechanisms from which metabolic acidosis is generated. Uncomplicated metabolic acidosis is manifested by an increase in blood acidity, hypobicarbonatemia, and hypocapnea. The magnitude of these changes defines the severity wf the acidosis. It is convenient to divide metabolic acidosis into two general categories (hyperchloremic and normochloremic), based on the observed anion gap, as this serves to narrow the differential diagnosis. The normal anion gap is that amount of plasma anion not measure by routine laboratory screening that accounts for the difference between the measured sodium cation (Na+) and anions (Cl +/- HCO3-). Metabolic acidosis; causes; diagnosis; clinical manifestations.

Acid-Base Imbalance↗

PubMedDate not supplied

Control of energy production in cardiac muscle: effects of ischemia in acidosis.

Evidence is summarized indicating that mitochondrial respiration and citric acid cycle activity in the intact heart are controlled by the cytosolic phosphate potential and mitochondrial NAD oxidation-reduction state. Data are presented showing that the effect of respiratory acidosis is greater than that of metabolic acidosis in inhibiting left ventricular pressure development in the perfused rat heart, because of a greater fall of intracellular pH under the former conditions. Respiratory acidosis is shown to be readily associated with tissue hypoxia as a result of an increased vascular resistance and diminished flow rate through the coronary circulation. In nonischemic respiratory acidosis, the rate of ATP production is well balanced by the rate of ATP utilization, and tissue ATP and creatine-P levels remain approximately normal. Partially ischemic respiratory acidosis was associated with low tissue levels of ATP and creatine-P and high tissue levels of lactate and NADH. Ischemic areas with sharp border zones were visualized during and after an abrupt decrease of perfusion fluid pH by directly photographing NADH fluorescence from the surface of perfused hearts. Reversal of the hypodynamic state with partially ischemic respiratory acidosis could not be achieved by augmenting the coronary flow by means of an external pump. The demonstration of the existence of sharp zones of high pyridine nucleotide fluorescence adjacent to normal zones indicates a great heterogeneity of coronary perfusion and the existence of steep oxygen gradients in the intact heart.

Acidosis↗

PubMed1978

Severe hyperchloremic acidosis complicating jejunoileal bypass.

In summary, severe hyperchloremic acidosis developed in two patients as a late complication after jejunoileal bypass for morbid obesity. This acidosis was associated with episodes of dizziness, ataxia, headache, weakness, confusion and transient loss of consciousness. Recognition of this symptom complex in the patient with a jejunoileal bypass should suggest metabolic acidosis as a complication of this surgical procedure. Bicarbonate replacement provided prompt, but temporary, improvement in the symptoms and the acidosis. Revision of the intestinal bypass was required for correction. Special studies to rule out renal tubular acidosis were performed and definitely excluded the kidney as a source of the acidosis.

Acidosis↗

PubMed1984

Effect of acidosis on bilirubin deposition in rat brain.

The effect of metabolic and respiratory acidosis on bilirubin and albumin entry into the brain was studied in 24 awake and unanesthetized rats. Hyperbilirubinemia was established by infusion of unconjugated bilirubin at a rate of 30 mg/kg/h for three hours. After two hours, metabolic acidosis was produced in eight rats by infusion of 0.5 N hydrochloric acid at a rate of 0.02 mL/g/h. This reduced the pH level to 7.03 +/- 0.01 (mean +/- SEM) with a normal value for PCO2. Respiratory acidosis was produced in another group of eight animals who breathed 20% CO2 in a balanced gas mixture for the last hour of the study period. This resulted in a reduction of pH to 7.04 +/- 0.01 with PCO2 of 100.4 +/- 2.3 mm Hg. A third group of eight rats served as controls and were given equal volumes of saline infusion. No increase in brain bilirubin or brain albumin was found in the group with metabolic acidosis, but in the group with respiratory acidosis both bilirubin and albumin concentrations in the brain increased significantly. No significant differences were found between the groups in serum total or apparent unbound bilirubin, albumin, or osmolality. The results indicate that a brief period of acidosis per se does not increase bilirubin entry into the brain, but hypercarbia does so by opening of the blood-brain barrier.

Acidosis↗

PubMed1998

Urinary net charge in hyperchloremic metabolic acidosis.

OBJECTIVE: (i) To examine the usefulness of urinary net charge (UNa + UK - UCl) in the evaluation of hyperchloremic metabolic acidosis secondary to diarrhea, distal RTA and proximal RTA and (ii) To characterize the type of distal RTA on the basis of the underlying defect. SETTING: Pediatrics division of a tertiary referral center. SUBJECTS: Thirty four children with hyperchloremic metabolic acidosis secondary to diarrhea (n = 16), distal RTA (n = 11) and proximal RTA (n = 7). Ten normal children with ammonium chloride induced acidosis were also studied. METHODS: All subjects underwent urine collection of 30-60 minutes duration for measurement of Na, K, Cl, pH and pCO2. The measurements were also made on the blood samples collected at the midpoint of urine collection. The urinary net charge was calculated by subtracting Cl values from the sum of the Na and K. RESULTS: Patients with proximal and distal RTA had a positive urine net charge. Patients with diarrhea and ammonium chloride induced acidosis showed negative urine net charge. Patients with diarrhea with extremely low urine sodium levels showed an inappropriately high urine pH despite persistent metabolic acidosis. All patients with distal RTA were found to have a secretory type of defect. CONCLUSION: Measurement of urine net charge is helpful in the initial evaluation of a patient with hyperchloremic metabolic acidosis.

Acidosis↗

PubMed1994

[Compensating for acidosis: pro].

New insights about the pathophysiology of acidosis as well as the efficacy of various buffer solutions have once again started the discussion about the necessity and indications of buffer therapy. After evaluation of the current literature one has to conclude that the spectrum of indications for application of buffer solution is remarkably small; some indications, however, remain well accepted. It has been shown that acidosis with pH-values above 7.2 has to be buffered only rarely, especially if the underlying disease responds to causal therapy. pH-values under 7.2, however, caused by renal tubular acidosis or by certain types of lactate acidosis, respond to buffer therapy. The choice of buffer solution depends on the pathophysiology of the underlying disease. In particular the application of CO2 generating buffer solutions under the conditions of critically reduced circulation and ventilation remains doubtful. Application of CO2 generating buffers seems to be justified only if intracellular acidosis can be prevented by immediate elimination of carbon dioxide generated by the buffer reaction.

Acid-Base Equilibrium↗

PubMed1992

Biguanide-associated lactic acidosis. Case report and review of the literature.

PURPOSE: The biguanides are a class of oral hypoglycemic agents that are commonly used in the treatment of diabetes mellitus. Such agents include metformin, phenformin, and buformin. The use of phenformin was discontinued in the United States in 1976 because of probable association with lactic acidosis. However, metformin is currently in common use in many parts of the world. In this report, we describe a patient with severe lactic acidosis secondary to metformin administration, and review the literature relevant to biguanide-associated lactic acidosis. PATIENT: We describe a diabetic man with end-stage renal failure and diabetes mellitus who was hospitalized with life-threatening lactic acidosis (lactate, 10.9 mmol/L). Unbeknownst to the hospital staff, he was being treated with metformin, which had been prescribed in Indonesia. RESULTS: Arterial blood gas analysis revealed a pH of 6.76 and a bicarbonate level of 1.6 mmol/L prior to treatment. Following therapy, which included oxygen, volume expansion, other supportive therapy, and hemodialysis, the patient completely recovered and was discharged from the hospital. CONCLUSIONS: Lactic acidosis can complicate biguanide therapy in diabetic patients with renal insufficiency. We review the literature relevant to the pathogenesis and therapy of biguanide-associated lactic acidosis. Physicians who have completed their training after 1976 may not be familiar with metformin and other biguanides, but with the increasing numbers of immigrants to the United States, physicians should be aware of the potential complications of these medications.

Acidosis, Lactic↗

PubMed2003

Risk of fatal and nonfatal lactic acidosis with metformin use in type 2 diabetes mellitus: systematic review and meta-analysis.

BACKGROUND: Metformin therapy for type 2 diabetes mellitus has been shown to reduce total mortality rates compared with other antihyperglycemic treatments but is thought to increase the risk of lactic acidosis. The true incidence of fatal and nonfatal lactic acidosis associated with metformin use is not known. METHODS: A comprehensive search was performed to identify all comparative trials or observational cohort studies published between January 1, 1959, and March 31, 2002, that evaluated metformin therapy, alone or in combination with other treatments, for at least 1 month. The incidence of fatal and nonfatal lactic acidosis was recorded as cases per patient-years for metformin treatment and for placebo or other treatments. In a second analysis, lactate levels were measured as a net change from baseline or as mean treatment values for metformin and comparison groups. RESULTS: Pooled data from 194 studies revealed no cases of fatal or nonfatal lactic acidosis in 36 893 patient-years in the metformin group or in 30 109 patients-years in the nonmetformin group. Using Poisson statistics with 95% confidence intervals, the probable upper limit for the true incidence of lactic acidosis in the metformin and nonmetformin groups was 8.1 and 9.9 cases per 100 000 patient-years, respectively. There was no difference in lactate levels for metformin compared with placebo or other nonbiguanide therapies. CONCLUSION: There is no evidence to date that metformin therapy is associated with an increased risk of lactic acidosis or with increased levels of lactate compared with other antihyperglycemic treatments if the drugs are prescribed under study conditions, taking into account contraindications.

Acidosis, Lactic↗