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PubMed1985

The effect of short term normothermic global ischemia and acidosis on cardiac myofibrillar Ca2+-Mg2+ ATPase activity.

There is now good evidence to indicate the onset of myocardial ischemia is accompanied by a decline in intracellular pH which parallels the decrease in tension development. The component of the excitation--contraction coupling system which is responsible for the loss in tension development has not been determined although the contractile proteins are a likely candidate since the calcium sensitivity of tension development and of myofibrillar ATPase are both inhibited by a decrease in pH. However, these studies have utilized normal tissues and the effects of pH compounded with ischemia have not been determined. It is plausible to suggest that there may occur ischemic damage to the excitation--contraction coupling system which would depress function in a manner distinct from that incurred by acidosis. Toya-Oka and Ross have demonstrated a loss in regulatory proteins during regional ischemia, suggesting an effect of ischemia independent of pH. We recently demonstrated, in sarcoplasmic reticulum isolated from ischemic myocardium, a defect in function which could not be accounted for solely on the decrease in pH. It was, therefore, the purpose of this study to determine the effects of decreasing pH on cardiac myofibrillar ATPase activity isolated from hearts which had been subjected to short-term, global normothermic ischemia. This design permits us to answer the following questions: Is there a decrease in myofibrillar ATPase activity in the canine heart following 30 min of normothermic global ischemia? Does acidosis play a contributory role in any observed depression of myofibrillar ATPase activity during ischemia? and Does the ischemic process, independent of acidosis, produce a further depression of myofibrillar ATPase activity?

Acidosis↗
PubMed1986

Triggered activity induced by combined mild hypoxia and acidosis in guinea-pig Purkinje fibers.

The effects of prolonged exposure to combined mild hypoxia (Po2 230 +/- 20 mmHg) and acidosis (pH: 6.8 +/- 0.05) were studied in guinea-pig left ventricular myocardium superfused in vitro. Only Purkinje fibers were impaled by microelectrodes. Triggered activity developed in depolarized Purkinje fibers after 48 +/- 9 min of exposure to hypoxic and acid conditions and was initiated either by short periods of rapid electrical driving or by the background slow Purkinje automaticity. Triggered activity occurred when a delayed afterdepolarization attained its threshold potential and terminated after a subthreshold afterdepolarization. Interaction between triggered activity and slow background automaticity was observed until 90 to 180 min of exposure to hypoxic and acid conditions. These effects were reversed by replacement in standard conditions (Po2 510 +/- 20 mmHg; pH 7.35 +/- 0.05). Norepinephrine (1 X 10(-6)M) significantly accelerated the rate of discharge of triggered foci and led to a stable sustained triggered activity. Increasing extracellular Ca2+ concentration aggravated the effects of combined mild hypoxia and acidosis and led to the occurrence of early afterdepolarizations initiating triggered activity. In addition abnormal automaticity developed in quiescent fibers without any triggering action potential. Lidocaine and verapamil suppressed the triggered activity following a subthreshold afterdepolarization. Their effects were reversed on wash-out. It is concluded that prolonged exposure to combined mild hypoxia and acidosis induces triggered activity by a basic mechanism common to other situations leading to a calcium overload and showing such behaviour.

Acidosis↗
PubMed1993

Urine-to-blood carbon dioxide tension gradient and maximal depression of urinary pH to distinguish rate-dependent from classic distal renal tubular acidosis in children.

We determined the prevalence and clinical features of rate-dependent distal renal tubular acidosis (dRTA) in 31 children examined for possible renal tubular acidosis by measuring the urinary-minus-blood partial pressure of carbon dioxide (U-B PCO2) gradient, minimal urinary pH, and fractional excretion of bicarbonate. Of 20 patients with low U-B PCO2 gradients, nine could not lower urinary pH < or = 5.5, indicating classic dRTA, whereas 11 could lower urinary pH < or = 5.5, as described in rate-dependent dRTA. When patients with rate-dependent dRTA and classic (type I) dRTA were compared, there was no difference in the mean U-B PCO2 gradient or in clinical findings, including age, reason for referral, presence of nephrocalcinosis, or depression of linear growth. We conclude that children with rate-dependent dRTA are susceptible to at least some of the same sequelae as children with classic dRTA. Measurement of minimal urinary pH will not detect this subtle form of dRTA. Determination of the U-B PCO2 gradient should be considered a routine part of evaluation for suspected renal tubular acidosis in a child.

Acidosis, Renal Tubular↗
PubMed1975

Renal tubular acidosis and skeletal demineralization in patients on long-term anticonvulsant therapy.

Three children ranging from seven to 12 years of age from unrelated families were given long-term anticonvulsant therapy including acetazolamide (Diamox). These children had rickets and renal tubular acidosis. Investigations have suggested (1) secondary hyperparathyroidism due to hypocalcemia of rickets and (2) prolonged acetazolamide therapy were responsible for acidosis as a result of reduction of bicarbonate reabsorption in the kidney. A clear-cut recovery from acidosis and rickets was seen in two patients following medication with high doses of vitamin D, an oral supplement of phosphorus, and discontinuance of acetazolamide therapy.

Acetazolamide↗
PubMed1983

D-Lactic acidosis in children: an unusual metabolic complication of small bowel resection.

Acidosis caused by intestinal bacterial D-lactate production occurs in ruminants engorged with carbohydrate. A similar phenomenon was identified in two children who developed recurrent episodes of metabolic acidosis and peculiar neurologic symptoms in response to increased dietary carbohydrate after major small bowel resections. Both children were found to have elevated plasma concentrations of D-lactic acid at the time of each episode. Acid base and neurologic abnormalities responded immediately to neomycin therapy. Among a number of microorganisms isolated from stool cultures of these patients, one anaerobic Lactobacillus acidophilus species produced large amounts of D-lactate in vitro. Reduction in carbohydrate intake in one patient tested led to a fall in D-lactate generation. We believe that excessive D-lactate production by intestinal bacteria, from malabsorbed carbohydrate, may produce metabolic acidosis and neurologic symptoms in children with small bowel resections.

Acidosis↗
PubMed1985

Prevention of recurrent calcium stone formation with potassium citrate therapy in patients with distal renal tubular acidosis.

Distal renal tubular acidosis is a common cause of intractable calcium nephrolithiasis. We examined the effect of oral potassium citrate therapy in 9 patients with incomplete distal renal tubular acidosis diagnosed on the basis of an abnormal response to an oral ammonium chloride load. Patients were studied during a control phase and after 3 months of potassium citrate treatment (60 to 80 mEq. daily). Potassium citrate caused a significant increase in urinary pH and urinary citrate, and a decrease in urinary calcium. The urinary relative saturation ratio of calcium oxalate significantly decreased during treatment, while that of brushite did not change. Potassium citrate also was shown to inhibit new stone formation. During a mean treatment period of 34 months none of the 9 patients had new stones, although 39.3 plus or minus 79.7 (standard deviation) stones per patient formed during the 3 years preceding treatment. The results support the potential clinical advantage of potassium citrate therapy in patients with distal renal tubular acidosis and recurrent calcium nephrolithiasis.

Acidosis, Renal Tubular↗
PubMed1979

Hyperchloremic acidosis and imperforate anus.

The predominant electrolyte imbalance associated with enterourinary fistulas is hyperchloremic acidosis. The mechanism is the absorption of urinary electrolytes across the colonic mucosa. One of the genitourinary associated anomalies of a high imperforate anus is a rectourinary fistula. There have been 5 cases of hyperchloremic acidosis as a complication of an imperforate anus with a rectourinary fistula reported in the literature to date. An additional case is presented with a clinical analysis of the previously reported cases. The important factors in the development of hyperchloremic acidosis in patients with an imperforate anus are 1) the presence of a rectourinary fistula, 2) an initial diverting colostomy permitting a long segment of colonic mucosa for the absorption of urinary electrolytes, 3) distal urinary tract obstruction allowing significant volumes of urine to flow into the colonic segment and 4) the presence of urinary tract infection contributing to the urinary obstruction. Management should consist of vigorous electrolyte therapy, decreasing the retrograde flow of urine into the colon by temporary catheterization and early repair of the fistulous tract.

Acidosis↗
PubMed1997

The effect of metabolic acidosis and alkalosis on the H+-ATPase of rat cerebral microvessels.

To determine the role of the proton translocating adenosine triphosphatase (H+-ATPase) of the blood-brain barrier, the density of the 31 Kd subunit of the vacuolar type H+-ATPase was quantitated in isolated rat cerebral microvessels with immunoblotting techniques. To establish the tissue specificity of the findings, synaptosomal membranes were also studied. Metabolic acidosis was induced with 1.5% ammonium chloride in drinking water for five days. Metabolic alkalosis was induced with 2.35% NaHCO3 in drinking water and daily injections of 10 mg/Kg furosemide intraperitoneally for 5 days. The quantity of the 31 Kd subunit (in arbitrary units) in cerebral microvessels was significantly increased in acidosis (3.98 +/- 0.45) (p<0.05) and was significantly decreased in metabolic alkalosis (0.49 +/- 0.16) (p<0.00) compared to controls (1.77 +/- 0.73). In synaptosomal membranes, metabolic alkalosis was associated with significant decrease in the quantity of the 31 Kd subunit-H+-ATPase (0.62 +/- 0.12 vs 0.92 +/- 0.01) p<0.05. The increase in the 31 Kd subunit in synaptosomal membranes with acidosis did not reach statistical significance. It is concluded that the quantity of vacuolar H+-ATPase in the blood-brain barrier is modulated by blood H+ or HCO3- content. These changes may be relevant to the physiology of the acid-base balance in the central nervous system.

Acidosis↗
PubMed1997

Possible synergistic effect of metformin and enalapril on the development of hyperkaliemic lactic acidosis.

A 71 year old hypertensive, non insulin-dependent diabetic patient with moderate renal insufficiency taking 500 mg/d of metformin and 5 mg/d of enalapril, developed metabolic acidosis characterized by fairly elevated anion gap, hyperchloremia, severe hyperkaliemia, normal plasma level of 3-hydroxybutyric acid, absence of ketonuria and high plasma level of lactic acid. This biochemical feature allowed us to ascribe the pathogenesis of metabolic acidosis, both to the increased plasma level of lactic acid and to the type IV renal tubular acidosis syndrome, the precipitating factor being an infection of urinary tract (as we assumed on the basis of the urine culture). The patient was dehydrated and lethargic; the ECG revealed the presence of nonparoxysmal junctional tachycardia. The clinical evolution was favorable under the treatment with an infusion of isotonic saline solutions, mild alkalinizing solutions, low-dose regular insulin and antibiotics. It is likely that metformin and enalapril, regularly taken by this nephropathic patient, could have played an iatrogenic role, even if the doses were low. This case highlights the importance of complying with the contraindications of these drugs, to avoid the rare but reported life-threatening complications of metformin administration.

Acidosis↗
PubMed1985

Lactic acidosis in fulminant hepatic failure. Some aspects of pathogenesis and prognosis.

To obtain further evidence of tissue hypoxia in fulminant hepatic failure, we have measured the mixed venous lactate concentration and the acid-base status of 32 patients at the time of their admission, in grade III or IV encephalopathy. The mixed venous lactate was elevated in 26 of the 32 patients (median 5.0 mmol/l, range 0.8-21.1 mmol/l), and, in 17 patients, this was associated with evidence of a metabolic acidosis. Mixed venous lactate levels correlated inversely with the mean arterial pressure (r = 0.56, P less than 0.005), systemic vascular resistance (r = 0.62, P less than 0.001) and the oxygen extraction ratio (r = 0.44, P less than 0.02). The 17 patients with a raised mixed venous lactate and metabolic acidosis had a significantly reduced systemic vascular resistance and oxygen extraction ratio compared with the other 15 (median systemic vascular resistances 944 and 1710 dyne X s/cm5/m2, respectively, P less than 0.05, median oxygen extraction ratios 19 and 23%, respectively, P less than 0.05). Survival was markedly reduced in the patients with hyperlactataemia and a metabolic acidosis, and only one out of the 17 survived compared with 12 of the remaining 15, P = 0.0002. These results suggest that lactic acid accumulation may be in part the consequence of tissue hypoxia that develops as a result of arteriovenous shunting, reflected in the reduction in systemic vascular resistance. This tissue hypoxia may occur despite apparently adequate systemic blood pressure, flow and oxygenation.

Acidosis↗
PubMed1991

Severe lactic acidosis following theophylline overdose.

The patient with theophylline overdose commonly presents with gastrointestinal, cardiovascular, neurologic, and electrolyte abnormalities. Respiratory alkalosis is the most common acid-base alteration, but mild metabolic acidosis has been reported. Two cases of severe lactic acidosis (pH 6.67 and 6.63) in patients without hypoxemia, shock, or prolonged seizure activity are reported. Possible causative mechanisms and aspects of therapy are discussed. Theophylline toxicity should be considered when an unconscious patient with concurrent severe metabolic acidosis presents to the emergency department.

Acidosis, Lactic↗
PubMed1984

Anion gap acidosis with hypoglycemia in acetaminophen toxicity.

Two case reports of patients with anion gap metabolic lactic acidosis and hypoglycemia are presented. Both patients subsequently died of acute liver failure secondary to acetaminophen hepatotoxicity. The development of type B lactic acidosis with hypoglycemia might have been caused by a deficit in gluconeogenesis secondary to severe hepatic failure and/or a toxic metabolite of acetaminophen. Our findings suggest that acetaminophen toxicity should be considered when lactic acidosis and hypoglycemia are seen.

Acetaminophen↗
PubMed1989

The effect of CO2 and non-CO2-generating buffers on cerebral acidosis after cardiac arrest: A 31P NMR study.

There is controversy regarding the use of alkalinizing agents during reperfusion after cardiac arrest. The potential deleterious effects of sodium bicarbonate (bicarb) administration, including paradoxic cerebral acidosis, have led to the search for alternative agents. Tromethamine (tris) is a non-CO2-generating buffer that has been proposed for use during cardiopulmonary resuscitation. The purpose of this experiment was to compare the ability of tris with bicarb to correct brain pH (pH B) during reperfusion after a 12-minute cardiac arrest. Adult mongrel dogs were instrumented and placed in the bore of a Bruker Biospec 1.89 tesla superconducting magnet system. Ventricular fibrillation was induced; after 12 minutes, cardiopulmonary bypass was initiated and maintained for two hours with minimum flows of 80 mL/kg/min. Bicarb (n = 5) or tris (n = 5) were administered to correct arterial pH as rapidly as possible. 31P NMR spectra were obtained at baseline and throughout ischemia and reperfusion. The pH B was determined with the inorganic phosphate relative to the phosphocreatine resonance signal shift. Profile analysis indicates a difference between groups (P less than .02) related to an initial delay in pH B correction in the tris group. By 48 minutes of reperfusion, pH B did not differ between the groups. Moreover, there was no evidence of paradoxic cerebral acidosis in the bicarb group. Although tris corrects blood pH as quickly as bicarb, it is less effective in correcting pH B. Absence of paradoxic acidosis may be caused by efficient elimination of CO2 by cardiopulmonary bypass.

Acidosis↗
PubMed1989

Severe metabolic acidosis after acute naproxen sodium ingestion.

Naproxen, a nonsteroidal anti-inflammatory drug (NSAID), is a propionic acid derivative that possesses analgesic and antipyretic properties through inhibition of prostaglandin synthesis. The propionic acids have been considered the least toxic of the NSAIDs, and one, ibuprofen, is currently available as an over-the-counter medication. Though acidosis has been reported with ibuprofen, no such occurrence has been reported for naproxen sodium. We report the case of a 15-year-old girl who presented with severe metabolic acidosis and seizures that rapidly followed naproxen sodium ingestion. Serum bicarbonate levels returned to normal 12 hours after admission and correlated with the known pharmacokinetics of naproxen. The pharmacokinetics of naproxen and treatment of its overdose, and possible mechanisms of metabolic acidosis are reviewed.

Acidosis↗
PubMed2000

Immunization with Streptococcus bovis protects against lactic acidosis in sheep.

Lactic acidosis is a gastrointestinal disorder resulting from the rapid overgrowth of lactic acid-producing bacteria when ruminants are suddenly introduced to grain feed. The present study has investigated the ability of live and killed bacterial vaccines to reduce lactic acidosis in sheep, via a stimulation of specific antibody production against lactic acid-producing bacteria. Forage-fed sheep were immunized with live or killed Streptococcus bovis Sb-5 vaccine, with or without adjuvant, via intramuscular injection. After the primary immunization, three boosters were given at 2-4 week intervals. Sheep were subsequently challenged by a sudden switch to a grain-based diet. Following challenge, vaccinated sheep maintained significantly higher feed intake, and had higher rumen pH, lower L-lactate concentrations, and less severe diarrhoea scores than non-vaccinated control sheep. Higher rumen pH, lower mortality and less severe diarrhoea were found in the animals immunized with live vaccine compared to the animals immunized with killed vaccines. Significant increases in mucosal and systemic antibody responses were observed after boosting; the S. bovis-specific antibody concentrations were significantly higher in samples of saliva, rumen fluid and serum from sheep immunized with live vaccine than with killed vaccines. These results demonstrate that lactic acidosis can be reduced by immunization against S. bovis, and that live Sb-5 vaccine is effective in invoking mucosal as well as systemic antibody responses.

Acidosis, Lactic↗
PubMed2000

Spurious metabolic acidosis in hemodialysis patients.

Metabolic acidosis with an increased anion gap (AG) is frequently seen among patients with end-stage renal failure that is corrected to a variable degree by chronic hemodialysis. The degree of acidosis is generally interpreted from the concentration of total carbon dioxide (tCO(2)) in blood drawn from the vascular access used for dialysis. As with many dialysis units in the United States, our laboratory studies for outpatients are performed in a central laboratory several hundred miles away and must be shipped there by air freight. We observed a consistent and clinically important difference between the tCO(2) content of samples reported from the central laboratory compared with results reported from a local university hospital chemistry laboratory. The central laboratory readings were always lower, resulting in an increase in the AG. Delays in centrifugation of the blood to separate the clot from the serum and in the initiation of analysis led to an increase in the lactate content of the samples. That increase, however, was insufficient to explain the difference in tCO(2) levels. These data suggest that something happens to the samples in transit to cause an artifactual reduction of the tCO(2) level. For many dialysis patients, the severity of their acidosis may be falsely represented by the tCO(2) content of blood samples reported from central laboratories.

Acidosis↗
PubMed1993

A model of the hyperkalemia produced by metabolic acidosis.

In both humans and animals, mineral acids predictably result in hyperkalemia, whereas plasma K+ remains normal or may even decrease during organic acidosis. The purpose of these studies was to define the mechanism for these effects in the opossum kidney cell, an established epithelial cell line derived from the renal cortex of the opossum. This cell was chosen because the acid/base transport pathways in this cell type are well defined and because it is one of the few cells known to express K/H antiport, the transport pathway that has been proposed to mediate the hyperkalemia of acidosis. Cell K+ at pH 7.4 averaged 988 +/- 48 nmol/mg protein. Relative to this value (100%), cell K+ increased when buffer pH was increased to pH 8.4 with NaOH (108% +/- 3%) and decreased when buffer pH was acidified with HCl to pH 6.4 (93% +/- 4%), producing a highly significant correlation of cell K+ with buffer pH: cell K+ (% of baseline at pH 7.4) = 6.9 (cell pH) + 49 (r = 0.5, P < 0.004). In contrast, acidification of the buffer to pH 6.4 with either butyric or lactic acid increased cell K+ (115% +/- 4% and 110% +/- 2%, respectively, both P < 0.05 v 7.4 or HCl value). Cell pH acidified in response to HCl at a rate of 0.0053 +/- 0.0007 pH U/s, a significantly slower rate than in response to lactic acid or butyric acid (0.0071 +/- 0.0007 and 0.0091 +/- 0.0007 pH U/s, respectively). Unidirectional ouabain-sensitive 42K+ influx was significantly inhibited by HCl acidosis and less so by the organic acids.(ABSTRACT TRUNCATED AT 250 WORDS)

Acidosis↗
PubMed1987

Absence of anion gap metabolic acidosis in severe methanol poisoning: a case report and review of the literature.

Methanol poisoning in humans is characterized by a latent period with subsequent development of anion gap metabolic acidosis and blindness. We describe a patient with potentially lethal methanol ingestion as evidenced by an admission serum methanol level of 403 mg/dL and sustained serum methanol levels greater than 50 mg/dL for more than 18 hours after ingestion, despite hemodialysis therapy. That anion gap metabolic acidosis or visual impairment did not develop in this patient was attributed to documented prior ethanol ingestion (admission serum ethanol level of 158 mg/dL) and continued ethanol administration during hospitalization (sustained serum ethanol levels greater than 100 mg/dL). This case demonstrates the ability of ethanol to inhibit the metabolism of methanol to formic acid in humans. This inhibition was achieved without induction of lactic acidosis. Thus this case documents the efficacy of ethanol therapy in patients with methanol poisoning.

Acid-Base Equilibrium↗