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Query: UMLS:C0847097 (acidity)
 15,165 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A basic premise in the utilization of the plasma anion gap in the assessment of acid-base disorders is that this parameter remains constant during hyperchloremic metabolic acidosis and metabolic alkalosis. Experimental data under in vitro conditions, however, cast serious doubt on this premise. The purpose of the present study was to characterize the plasma anion gap, estimated as (Na + K) - Cl + HCO3), in two large groups of dogs with graded degrees of chronic, HCl-induced metabolic acidosis or chronic, diuretic-induced metabolic alkalosis. The data indicate that the plasma anion gap decreases significantly in HCl acidosis and increases significantly in metabolic alkalosis; the predicted mean anion gap in animals with a plasma bicarbonate concentration of 10, 21 (normal), and 40 meq/liter approximated 13, 18, and 26 meq/liter, respectively. The observed variation in the plasma anion gap is interpreted as originating mainly from directional changes in the net negative charge of plasma proteins; these changes result from the titration process secondary to the altered plasma acidity and, in the case of metabolic alkalosis, from the additional effect of an increased plasma protein concentration.
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PMID:Changes in the plasma anion gap during chronic metabolic acid-base disturbances. 2 93

Metabolic acidosis is common in babies fed cows' milk-based formulae. Therefore the effects of adding alkaline salts (sodium and potassium citrate) to a demineralised whey formula were studied in vitro and in 26 low birthweight babies fed on the formula or formula plus citrate. The alkali altered the pH and titratable acidity to a value nearer human milk but it increased the buffering capacity to a value further away. This may effect the bacterial flora of the intestine. The babies fed on formula plus citrate did not make greater gains in weight, length, head circumference, skinfold thickness, or midarm muscle circumference, although they had a greater blood base excess. Some of these babies developed a mild metabolic alkalosis and 3 had hyponatraemia despite their increased sodium intakes. These babies also had lower levels of plasma transferrin but showed no differences in urea, albumin, cholesterol, and calcium levels. No baby fed on the demineralised whey formula without added citrate had a base deficit exceeding 5 mmol/l; late metabolic acidosis is less common in babies fed on this formula and the routine addition of alkali can have untoward metabolic effects.
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PMID:Milk pH, acid base status, and growth in babies. 3 63

It is uncertain whether, in humans, potassium depletion can cause or sustain metabolic alkalosis of clinically important degree in the absence of coexisting known alkalosis-producing conditions. Previously we found, in normal humans ingesting abundant NaCl, that dietary K+ depletion alone can induce and sustain a small decrease in blood acidity and increase in plasma bicarbonate concentration; we hypothesized that more severe alkalosis was prevented by mitigating mechanisms initiated by renal retention of dietary NaCl that was induced by K+ depletion. To ascertain the acid-base response to dietary K+ depletion under conditions in which the availability of NaCl for retention is greatly limited, in the present study of six normal men we restricted dietary K+ as in the previous study except that intake of NaCl was maintained low (2 to 7 mEq/day, Low NaCl Group) instead of high (126 mEq/day, High NaCl Group). Plasma acid-base composition and renal net-acid excretion (NAE) did not differ significantly between groups during the control period. In the steady state of K+ depletion (days 11 to 15 of K+ restriction), neither plasma K+ concentration (2.9 +/- 0.9 mEq/liter vs. 3.0 +/- 0.1 mEq/liter) nor cumulative K+ deficit (399 +/- 59 mEq vs. 466 +/- 48 mEq) differed significantly between groups. During K+ restriction, persisting metabolic alkalosis developed in both groups, which was more severe in the Low NaCl Group: increment in [HCO3-]p, 7.5 +/- 1.0 mEq/liter versus 2.0 +/- 0.3 mEq/liter, P less than 0.001; decrement in [H+]p, 5.5 +/- 0.6 nEq/liter versus 2.9 +/- 0.4 nEq/liter, P less than 0.003. A significantly more severe alkalosis in the Low NaCl Group was evident at all degrees of K+ deficiency achieved during the course of the 15 days of K+ restriction, and the severity of alkalosis in the Low NaCl Group correlated with the degree of K+ deficiency. During the generation of alkalosis (days 1 to 7 of K+ restriction), NAE increased in the Low NaCl Group whereas it decreased in the High NaCl Group. During the maintenance of alkalosis (days 11 to 15), NAE stabilized in both groups after it returned to values approximating the control values. In both groups, urine Cl- excretion decreased during K+ restriction even though Cl- intake had not been changed, with the result that body Cl- content increased negligibly in the Low NaCl Group (28 +/- 6 mEq) and substantially in the High NaCl Group (355 +/- 64 mEq).(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Dietary NaCl determines severity of potassium depletion-induced metabolic alkalosis. 303 34

Acute metabolic acidosis potentiates the nephrotoxicity of aminoglycosides by impairing the adequate excretion of ammonium and titratable acidity. The present study assesses distal tubular function after aminoglycoside administration in the rat. Two aminoglycosides, gentamicin and netilmycin were given to rats either in low doses equivalent to those used clinically (BG4 and BN5 groups) or in doses ten times higher (BG40 and BN50). The rats were subjected to acute metabolic alkalosis and the pCO2 of urine was continuously evaluated. The regression lines obtained by plotting the differences between urine and blood pCO2 as a function of urinary HCO3- in low dose models were similar to those obtained for the control group. However, the slopes obtained for BG40 and BN50 were significantly different from the control, suggesting an impairment of H+ secretion.
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PMID:Evaluation of distal tubular function in aminoglycoside-induced nephropathy. 313 93

In 27 infants aged 20 to 65 days with clinically and roentgenologically proved hypertrophic pyloric stenosis gastric juice analyses were performed according to Lambling. Basic acid output and maximal acid output in these infants were significantly increased as compared to healthy infants of the same age group. The higher acid output in the hypertrophic pyloric stenosis group was due to higher volumes and a higher acidity of the gastric juices. Basic acid output and maximal acid output increased following pylorotomy. There is evidence, that hyperacidity in pylorus stenosis of infancy is primarily and not due to the pyloric constriction. There was a distinct correlation between the degree of metabolic alkalosis and diminished acid outputs. The findings support the thesis, that infantile hypertrophic stenosis is originated by an increased parietal cell mass. The increased acid secretion and the enhanced release of secretin and cholecystokinin are supposed to originate the hypertrophy of the pyloric muscle.
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PMID:[Results of Lambling gastric juice analysis in infants with spastic hypertrophic pyloric stenosis (SHPS)]. 373 14

In the normal human body, the extracellular fluid pH of 7.40 is closely protected. Any increase in acidity or alkalinity summons forth three lines of defense, starting immediately with the blood buffers, followed soon by the respiratory system's control of CO2, and finally purged by the renal excretion of the excess acid or base. The complex interrelated processes of the renal responses require a few days to accomplish maximum compensation. We have presented the fundamental principles governing maintenance of the acid-base equilibrium to provide a conceptual framework for understanding the clinical disorders of hydrogen ion metabolism. The somewhat elusive concepts of endogenous acid production and net acid balance have also been reviewed to help reveal the pathophysiology of metabolic acidosis caused by renal tubular acidosis, chronic renal failure, certain infant feedings, and total parenteral nutrition. The development and perpetuation of metabolic alkalosis in relationship to chloride and potassium deficiency have been examined. In the delineation of a clinical acid-base disorder, the clinician must bear in mind the continual interactions of electrolytes and hormonal systems and should be prepared to reevaluate frequently the elected therapy against the changing responses, based on a thorough understanding of physiology. The various types of renal tubular acidosis have manifold facets but the basic understanding of their pathophysiology begins with the concept of the "anion gap," a point of reference that can be used in the differential diagnosis and treatment. In this chapter a number of new causes of type IV renal tubular acidosis--currently considered to be the most common form of renal tubular acidosis--have been pointed out, along with special reference to the mineral, electrolyte, and aldosterone metabolism in the various acidoses and current means of reversing growth failure in the child, especially through bicarbonate treatment. The mechanism of metabolic acidosis in chronic renal failure including metabolic acidosis in children undergoing dialysis and in recipients of kidney transplantation, and its relationships to mineral and electrolyte metabolism have been presented. The pathophysiology of the acidosis related to certain infant formulas and the acidogenic properties of some amino acid solutions employed in total parenteral nutrition have been briefly reviewed. Finally, the metabolic alkalosis seen in a variety of chloride deficiency syndromes, such as Bartter's syndrome and dietary chloride deprivation, has been discussed and a rational approach to evaluation and treatment outlined.
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PMID:Acid-base disorders and the kidney. 642 18

The stability of amino acids and the availability of acid from total parenteral nutrition (TPN) solutions containing hydrochloric acid were studied. Hydrochloric acid in the concentrations of 40 (TPN 1), 60 (TPN 2), and 100 (TPN 3) meq/liter was added to TPN solutions (4.25% amino acids, 25% dextrose monohydrate) containing various electrolytes (TPN control). Amino acid concentrations were determined from one sample of each solution using a Technicon Automatic Amino Acid Analyzer. Samples were analyzed 24 hours after mixing and compared with the TPN control at 24 hours. Tryptophan was assayed using a specific colorimetric assay at 0, 6, 24, and 48 hours. The concentrations of proline (76.2 of control) and histidine (85.7% of control) wee decreased in TPN 3. This phenomenon appeared to be dependent upon the concentration of hydrochloric acid in the TPN solution. There was no appreciable loss of any of the other amino acids in the test solution as compared with the control. Tryptophan levels fell in both the TPN control and the test solutions independent of the hydrochloric acid concentration. The pH of the solutions decreased with increasing concentrations of hydrochloric acid from 5.87 in the TPN control to 3.18 in TPN 3. The titratable acidity increased with increasing concentrations of hydrochloric acid (28.21 meq/liter in the TPN control to 115.54 meq/liter in TPN 3). Concentrations of some amino acids decreased in the presence of hydrochloric acid. Because of the short-time period in which these solutions will usually be infused (4-24 hours), this probably has a negligible effect on patients' nutritional therapy. The availability of acid from these solutions makes this combination useful in treating severe metabolic alkalosis.
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PMID:Stability of amino acids and the availability of acid in total parenteral nutrition solutions containing hydrochloric acid. 679 23

Using the cold restrained rat model of stress ulceration, we have examined the influence of metabolic acidosis, metabolic alkalosis, and respiratory acidosis on the development of gastric erosions. The rats were restrained in tightly fitting perspex chambers at 6 degrees C for 3 hours. Acid-base imbalance was achieved by infusion of NH4Cl or NaHCO3 or by exposure to 5% CO2. The degree of ulceration was expressed by a lesion score of 0 to 4. The control group showed a score of 2.5 +/- 0.2 (mean +/- SEM). With metabolic acidosis the score was 3.6 +/- 0.2, and with metabolic alkalosis the score was 0.9 +/- 0.4. Both values were significantly different from control values (P less than 0.005). Respiratory acidosis was associated with a score similar to that of the control group. The values obtained appeared to be independent of gastric luminal acidity. The findings indicate that the systemic HCO-3 concentration is a significant determinant of the degree of ulceration in the cold restrained rat.
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PMID:Acid-base imbalance and ulceration in the cold restrained rat. 705 14

Exposure to hyperoxia (500-600 torr) or low pH (4.5) for 72 h or NaHCO(3) infusion for 48 h were used to create chronic respiratory (RA) or metabolic acidosis (MA) or metabolic alkalosis in freshwater rainbow trout. During alkalosis, urine pH increased, and [titratable acidity (TA) - HCO(-)(3)] and net H(+) excretion became negative (net base excretion) with unchanged NH(+)(4) efflux. During RA, urine pH did not change, but net H(+) excretion increased as a result of a modest rise in NH(+)(4) and substantial elevation in [TA - HCO(-)(3)] efflux accompanied by a large increase in inorganic phosphate excretion. However, during MA, urine pH fell, and net H(+) excretion was 3.3-fold greater than during RA, reflecting a similar increase in [TA - HCO(-)(3)] and a smaller elevation in phosphate but a sevenfold greater increase in NH(+)(4) efflux. In urine samples of the same pH, [TA - HCO(-)(3)] was greater during RA (reflecting phosphate secretion), and [NH(+)(4)] was greater during MA (reflecting renal ammoniagenesis). Renal activities of potential ammoniagenic enzymes (phosphate-dependent glutaminase, glutamate dehydrogenase, alpha-ketoglutarate dehydrogenase, alanine aminotransferase, phosphoenolpyruvate carboxykinase) and plasma levels of cortisol, phosphate, ammonia, and most amino acids (including glutamine and alanine) increased during MA but not during RA, when only alanine aminotransferase increased. The differential responses to RA vs. MA parallel those in mammals; in fish they may be keyed to activation of phosphate secretion by RA and cortisol mobilization by MA.
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PMID:Renal responses of trout to chronic respiratory and metabolic acidoses and metabolic alkalosis. 1044 55

OBJECTIVE: To investigate the classification and incidence of acid-base disturbance (ABD) in the patients with post-traumatic multiple organ dysfunction syndrome (MODS). METHODS: A total of 119 patients with MODS were examined with arterial blood gas analysis and serum electrolytes detection for 675 times in this study. RESULTS: Different types of ABD existed in 647 times out of 675 times (95.9%) of blood-gas analyses. There were 270 times (41.7%) of simple ABD, 271 times (41.9%) of double ABD and 106 times (16.4%) of triple ABD. Among which, 404 times (62.4%) were in respiratory alkalosis (RAL), 332 times (51.3%) in metabolic acidosis (MA), 227 times (35.1%) in metabolic alkalosis (MAL) and 167 times (25.8%) in respiratory acidosis (RA). In this study, 79 cases (66.4%) out of 119 cases with MODS died from these kinds of ABD. CONCLUSIONS: It suggests that in the early stage of MODS, RAL with or without hypoxemia may exist, and later on, MA or even triple ABD may occur. In order to detect and correct the primary disorders as early as possible, it is important to keep the balance of hydrolyte. The treatment of primary diseases is also important. Disorders of acid-base balance were corrected according to pH standard values, anion gap (AG) and the potential [HCO(3)(-)] were also calculated simultaneously. When pH was more than 7.50 or lower than 7.20, it is necessary to give drugs of acidity or alkalinity to the patients with ABD to maintain pH value within a normal range.
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PMID:Study on acid-base disturbance in patients with post-traumatic multiple organ dysfunction syndrome. 1187 52


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