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PubMed1977

[Acid production and the need for bicarbonate in diabetic acidosis].

In a study of 54 patients with diabetic keto-acidosis with pH on admission less than or equal to 7.1, the amount of bicarbonate (HCO3-) necessary to correct the acidosis is compared to the amount predicted by the formula HCO3- (MEq) = 0,3 X body weight (kg) KG) X delta base excess (mEq/l). HCO3- requirements vary widely among patients. In addition, whenever HCO3- is given within 1-2 h the requirement may be inferior to the value calculated, whereas with slow HCO3- infusion it can be twice or three times the amount calculated. Variable HCO3- needs among subjects, and increased needs with time, are due to acid production which may exceed 100 mEq/h, especially in young patients. The amount of HCO3- required is determined not only by the severity of acidosis but also by net acid production, which may vary widely. The assessment of acid-base balance during treatment is useful in evaluating the amount of acid produced and hence the precise need for HCO3- replacement.

Acid-Base Equilibrium↗
PubMed1972

Lactic acidosis with phenformin therapy.

Nine cases of severe acidosis occurring in patients with maturity onset diabetes who were receiving phenformin therapy were reviewed. All had evidence of renal disease. Lactic acidosis was diagnosed by elevated blood lactate levels in seven patients, and by the clinical manifestations and laboratory information in the other two. Contributing factors are discussed, as well as means of treatment and prevention. Although the specific etiology of renal disease is not emphasized in this paper, unrecognized progressive deterioration of renal function is implicated in the etiology of lactic acidosis.

Aged↗
PubMed1976

Lactic acidosis in diabetic patients.

Plasma lactate and beta-hydroxybutyrate concentrations were measured during episodes of ketoacidosis and lactic acidosis in diabetics. In 39 patients with ketoacidosis, with a mean plasma beta-hydroxybutyrate concentration of 12.4 millimols/liter, the plasma lactate concentration was less than 3.6 millimols/liter in 28 and moderately elevated in 11. In seven of the latter, coexisting lactic acidosis had been suspected clinically. In these 39 patients, there was no correlation between plasma lactate and beta-hydroxybutyrate concentrations. In six of ten episodes of presumed and later proved lactic acidosis, despite negative or weakly positive serum reactions with sodium nitroprusside, the plasma beta-hydroxybutyrate concentration was elevated. Although positive, the serum reaction with nitroprusside was also misleadingly weak in five of 39 patients with ketoacidosis, including three with plasma lactate concentrations less than 3 millimols/liter.

Adult↗
PubMed1983

Acidosis alters fluorescein permeability. Differential tracer penetration through pigment epithelium.

The permeability of the blood-retinal barrier to infusion of fluorescent tracers was examined in tissue sections of frozen eyes from conscious rats that had breathed either air (control) or 25% carbon dioxide in air for one hour. For all animals the blood-retinal barrier remained impermeable to either carboxyfluorescein or Evans blue, indicating a functionally intact tight junctional barrier during hypercapnia. However, in hypercapnic animals, fluorescein penetrated into the neural retina, mainly via the pigment epithelium. Fluorescein also passed through the pigment epithelium in rats with metabolic acidosis induced by intravenous infusion of ammonium chloride, which lowered arterial blood pH without raising the Paco2 or BP. The results indicate an increased permeability of fluorescein through the cell membranes of the pigment epithelium during respiratory and metabolic acidosis. The effect on fluorescein may be due to a pH-dependent increase in the plasma concentration of the associated, more lipid-soluble form of this weak acid.

Acidosis↗
PubMed1984

Acetazolamide teratogenesis: interaction of maternal metabolic and respiratory acidosis in the induction of ectrodactyly in C57BL/6J mice.

Exposure of C57BL/6J mice to 20% CO2 for 8 hours on day 10 of gestation has been shown to produce right-sided postaxial forelimb ectrodactyly in 23% of the offspring. Carbon dioxide exposure produces a dramatic increase in maternal plasma CO2 accompanied by an inevitable decrease in plasma pH, both of which appear to be involved in the induction of ectrodactyly. However, the low incidence of ectrodactyly associated with NH4Cl-induced metabolic acidosis suggests that the primary teratogenic factor in respiratory acidosis is elevated CO2 tension. This conclusion is supported by the observation that moderation of maternal plasma pH in the face of sustained elevated PCO2 fails to reduce the incidence of ectrodactyly; moreover, there is a strong correlation between maternal serum CO2 content and the incidence of ectrodactyly.

Abnormalities, Drug-Induced↗
PubMed1978

Sodium wasting, acidosis and hyperkalemia induced by methicillin interstitial nephritis. Evidence for selective distal tubular dysfunction.

A 61 year old male patient was studied who manifested dehydration, azotemia, acidosis and hyperkalemia six weeks after exposure to methicillin. Thyroid and adrenal glucocorticoid and mineralocorticoid function were normal. The dehydration was found to be caused by a profound sodium-losing nephropathy; urinary sodium ranged from 78 to 101 meq/day during a salt restricted diet. A distal renal tubular acidosis and a quantitively impaired ability to excrete potassium were also found. These defects were relatively unresponsive to mineralocorticoid or prednisone therapy. A renal biopsy specimen showed an interstitial nephritis which selectively affected distal tubules and was thought to be secondary to methicillin. The data suggest functional impairment specific for the distal tubule, but with only a modest decrease in the glomerular filtration rate.

Acidosis↗
PubMed1988

Effects of respiratory and metabolic alkalosis and acidosis on pipecuronium neuromuscular block.

Acute respiratory and metabolic acidosis as well as metabolic alkalosis increased (by 11, 11, 21%) whereas respiratory alkalosis antagonized (by 10%) the partial steady state block produced by pipecuronium infusion on the anterior tibialis muscle of the cat. The duration of neuromuscular block following six successive doses of pipecuronium was prolonged 1.4-fold during long-lasting metabolic alkalosis while this parameter was shortened to half of that in control cats during acidosis. Pipecuronium block could be fully antagonized by neostigmine.

Acidosis↗
PubMed2002

Metabolic acidosis in the intensive care unit.

Metabolic acidosis is a common occurrence in critically ill patients. Understanding the pathological mechanisms underlying the generation of protons will enable the clinician to quickly recognize these disorders and establish an acceptable treatment strategy. This article presents a logical approach to metabolic acidosis.

Acid-Base Imbalance↗
PubMed1995

Osteoblastic intracellular pH and calcium in metabolic and respiratory acidosis.

In vitro metabolic acidosis (Met) induces greater bone mineral resorption than respiratory acidosis (Resp). Met, but not Resp, inhibits osteoblasts which control many aspects of osteoclastic function. To determine whether at a similar decrement in extracellular pH, Met and Resp would induce different changes in intracellular pH (pHi) and/or intracellular calcium concentration ([Ca2+]i) of osteoblasts, we measured pHi and [Ca2+]i in an osteoblast-like rat osteosarcoma cell line (UMR-106). Cells were grown to confluence on glass slides and loaded with either 1.5 microM BCECF, for pHi, or 1.5 microM Fura-2, for [Ca2+]i, in control (Ctl; pH approximately 7.40, PCo2 approximately 40, [HCO3-] approximately 24) medium. The fluorescence ratio at excitation wavelengths of 502 and 440 nm was measured for pHi and at 340 and 380 nm for [Ca2+]i. Following a baseline scan in Ctl medium, cells were transferred to either Met (pH approximately 7.10, PCo2 approximately 40, [HCO3-] approximately 12), Resp (pH approximately 7.10, PCo2 approximately 80, [HCO3-] approximately 24) or Ctl conditions. Medium pH, PCo2 and [HCO3-] were held constant over the course of the experiment. Compared to Ctl, pHi was lower in Met (P < 0.001) and even lower in Resp (P < 0.001 vs. Met and vs. Ctl). These changes were maintained over the period of observation. Compared to Ctl, [Ca2+]i was higher in Met (P < 0.001) and even higher in Resp (P < 0.001 vs. Met and vs. Ctl) within 20 to 100 seconds. However, after 100 seconds [Ca2+]i was not different in the three groups.(ABSTRACT TRUNCATED AT 250 WORDS)

Acidosis↗
PubMed1995

Cardiovascular responses to graded doses of three catecholamines during lactic and hydrochloric acidosis in dogs.

We have studied the cardiovascular effects of incremental doses of three catecholamines in dogs subjected to lactic (LAC) and hydrochloric (HCl) acidosis. Fifty-four dogs were allocated randomly to one of three groups: control, LAC and HCl acidosis (n = 18 each group). In the acidotic models, 2 mol litre-1 of lactic acid (4 ml kg-1 h-1) or 2 mol litre-1 of HCl (1 ml kg-1 h-1) was infused i.v. until arterial pH was reduced to 7.00 +/- 0.1. Within each group, six dogs received one of three different drugs in logarithmically incremental doses: adrenaline 0.1, 0.2, 0.4, 0.8, 1.6, 3.2 micrograms kg-1 min-1, noradrenaline 0.1, 0.2, 0.4, 0.8, 1.6, 3.2 micrograms kg-1 min-1 and dobutamine 5, 10, 20, 40, 80, 160 micrograms kg-1 min-1. Cardiovascular variables were monitored, with periodic measurements of plasma electrolyte and lactate concentrations. The pH reduction induced by HCl or lactic acid was associated with a statistically significant increase in mean pulmonary arterial pressure (MPAP), prominent especially in the LAC group where MPAP increased from mean 18 (SD 5) to 27 (6) mm Hg. In the acidotic models, the reduction in myocardial responsiveness to adrenaline or noradrenaline was more prominent than that for the control for corresponding doses of drugs. In the LAC group mean cardiac index decreased significantly from 5.2 (1.8) to 2.2 (0.7) litre min-1 m-2 after infusion of adrenaline 3.2 micrograms kg-1 min-1 and decreased from 5.1 (1.1 to 2.4 (0.9) litre min-1 m-2 after infusion of noradrenaline 3.2 micrograms kg-1 min-1.(ABSTRACT TRUNCATED AT 250 WORDS)

Acidosis↗
PubMed1990

Effect of acidosis and alkalosis on postischemic Ca gain in isolated rat heart.

The effect of pH of the reperfusion buffer on postischemic changes in tissue Ca and Na was examined in isolated Langendorff-perfused Sprague-Dawley rat hearts. Reperfusion began after 15-, 25-, or 60-min ischemia at 37 degrees C. After 60-min ischemia, reperfusion at pH 6.4 or 6.6 attenuated the reperfusion-induced Ca gain so long as the acidotic conditions were maintained (3.08 +/- 0.22, 1.37 +/- 0.41, and 16.96 +/- 1.18 mumol Ca gain/g dry wt for pH 6.4, 6.6, and 7.4, respectively after 15-min reperfusion). Conversely, reperfusion under alkalotic conditions (pH 7.9) after 60-min ischemia exacerbated the gain (27.45 +/- 4.75 and 8.92 +/- 1.53 mumol Ca gain/g dry wt during 5-min reperfusion at pH 7.9 and 7.4, respectively). Similar, but less pronounced Ca gains occurred during reperfusion after 15- or 25-min ischemia. Sodium content during reperfusion, but not during aerobic perfusion, was also found to be pH sensitive with acidosis causing a reduction and alkalosis an increase. These results could not be explained in terms of an effect of pH on recovery of high-energy phosphates, percentage "reflow" during reperfusion, or reperfusion-induced increases in tissue water or resting tension. The results are in agreement with the hypothesis that the "inhibitory" effect of acidosis on postischemic Ca overload could involve an effect of pH on the Na(+)-H+ exchanger and intracellular Ca storage.

Acidosis↗
PubMed1983

Effect of respiratory acidosis on acidification by the medullary collecting duct.

The effect of acute respiratory acidosis (ARA) on inner medullary collecting duct (IMCD) acidification was studied and the results were compared with previously obtained data by our laboratory in rats with acute metabolic acidosis (AMA). We employed the microcatheterization technique to directly measure pH and PCO2 with glass-membrane electrodes, and fluid samples were obtained for measurement of bicarbonate, phosphate, and ammonium. Arterial pH was 7.18 +/- 0.01 and PCO2 was 88 +/- 2 mmHg. The IMCD data were analyzed as a function of IMCD length (approximately 6 mm). pH decreased from 5.78 +/- 0.07 to 5.27 +/- 0.03 and PCO2 increased from 55 +/- 4 to 75 +/- 2 mmHg between origin and tip. Bicarbonate delivery decreased from 154 +/- 34 to 25 +/- 3 nmol/min but no change was noted in acid phosphate, ammonium, or net acid addition along the IMCD. However, net acid excretion was not different from that found previously in AMA. We conclude that during ARA acidification is augmented prior to, but not along, the IMCD. In contrast, during AMA we previously found that IMCD plays a major regulatory role in urinary acidification, accounting for about 50% of the excreted hydrogen ion.

Acidosis↗
PubMed1975

Effect of correction of metabolic acidosis on bone mineralisation rates in patients with renal osteomalacia.

The role of metabolic acidosis in the genesis of renal osteomalacia was investigated by studying bone mineralisation and resorption rates with a combined isotope and balance technique in six patients, before and after the administration of alkali. Correction of blood pH was achieved in five cases and was associated with a significant rise in the bone mineralisation rates and a significant positive trend in the calcium balances. It is suggested that acidosis contributes to the pathogenesis of osteomalacia in renal failure by slowing skeletal mineralisation, possibly by inhibiting bone alkaline phosphatase.

Acidosis↗
PubMed1975

Depression of human myocardial contractility with "respiratory" and "metabolic" acidosis.

The effect of a similar degree of "respiratory" and "metabolic" acidosis was studied in seven isolated in vitro human pectinate muscles and eight ventricular muscle bundles. Either "respiratory" or "metabolic" acidosis (from 7.36 plus or minus 0.03 to 7.01 plus or minus 0.02 and 6.98 plus or minus 0.03, respectively) depressed in vitro contractility in human atrial or ventricular muscle to a similar extent. Previous contradictory responses of myocardial tissue to alterations in pH appear to be the result of species differences.

Acidosis↗
PubMed1977

Metabolic acidosis and alkalosis.

The factors controlling renal bicarbonate reabsorption and acid excretion under normal conditions and in the presence of metabolic acidosis and alkalosis are reviewed. The methods used to assess distal acidification and its limitations are also discussed. Measurement of urinary pCO2 in maximally alkaline urine (pH greater than 7.8) is a very useful qualitative method to assess distal acidification. The finding of a low urinary pCO2 in maximally alkaline urine indicates a distal acidification defect. We propose that both the secretory and gradient defect types of distal renal tubular acidosis are associated with a low urinary pCO2 when the urine is maximally alkaline. Sodium sulfate and neutral phosphate infusion may allow distinction between a secretory and gradient defect. Sodium sulfate lowers urine pH in the gradient defect but fails to produce the same response in the secretory defect. Neutral phosphate infusion when urine pH (6.8-7.4) is close to the pK of phosphate (6.8) results in an increase in urinary pCO2 in the gradient defect but not in the secretory defect. The mechanisms of generation, maintenance and treatment of metabolic alkalosis are also discussed.

Acidosis↗
PubMed1987

Carbicarb: an effective substitute for NaHCO3 for the treatment of acidosis.

Carbicarb (Na2CO3 0.33 molar NaHCO3 0.33 molar), a mixture formulated to avoid the objections to sodium bicarbonate therapy, has been compared with 1 mol/L NaHCO3 and 1 mol/L NaCl in the treatment of mixed respiratory and metabolic acidosis (pH 7.17) produced by asphyxia in rats. In clinically appropriate doses, intravenous NaHCO3 raised arterial pH only 0.03 unit, elevated arterial carbon dioxide pressure, and doubled lactate concentration. With Carbicarb, the pH rise was three times as great and the blood lactate level was unchanged. The new drug should be effective in treating the acidosis of cardiopulmonary failure without raising blood carbon dioxide pressure or lactate levels and at lower sodium doses than required for NaHCO3.

Acidosis, Lactic↗
PubMed1986

Metabolic acidosis as a presenting feature in acute asthma.

Acid-base abnormalities in adults with acute asthma are highly variable. The major abnormalities have been attributed to changes in PaCO2 secondary to altered alveolar ventilation. Primary metabolic alterations have been thought to be rare in adults. The frequency of metabolic acidosis in acute asthma was reevaluated by way of a review of the medical records of 164 hospitalizations involving 109 adults. The hydrogen ion concentration varied widely and in 27 of 164 episodes (16.5%) the arterial pH was lower than expected for the measured PaCO2. We conclude that the presenting acid-base status of adults with acute asthma is highly variable and metabolic acidosis is not an infrequent finding.

Acidosis↗
PubMed1987

[Hypoxia, acidosis and nephrology].

In a survey the correlations between hypoxia, acidosis and nephrology are presented. In chronic oxygen deficiency the individual aspects concern the uncertainties of erythropoietin and the carotid-sinusoidal natriuresis stimulated by chemoreceptors. The effects of acute ischaemic hypoxic reactions are described with regard to the acute renal failure. The regulatory renal function of acidification and its disturbance in chronic renal insufficiency as well as the renotubular acidosis are discussed. Finally the authors enter the influence on the renal function during positive pressure respiration (e.g. for the purpose of the normalisation of the pulmonary gas exchange in acute respiratory insufficiency) as well as on reactions of the haemodialysis (bicarbonate and acetate dialysis) to the blood gas and acid-base metabolism, taking into consideration the pulmonary function.

Acid-Base Equilibrium↗