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[Metabolic alkalosis].

Metabolic alkalosis (MA) only occurs after bicarbonate administration if given quickly and massively, or in the presence of renal failure. Most cases of MA are caused by a loss of hydrogen ions. This paper reviews the common causes (gastric aspiration, chronic diuretic therapy) and updates the list of drugs which may lead to this complication. Rare causes (such as hyper mineralo-corticoid secretion) should be suspected in patients with MA unresponsive to usual doses of potassium chloride. Hydrochloric acid infusions are reserved for very special cases.

Alkalosis↗

Experimental model of hypochloremic metabolic alkalosis caused by diversion of abomasal outflow in sheep.

Hypochloremic metabolic alkalosis accompanied by hypokalemia and hyponatremia was induced experimentally in 7 adult sheep by diversion (loss) of gastric contents through an Ivan and Johnston cannula placed in the cranial part of the duodenum just distal to the pylorus. Cannula placement was easily accomplished, and cannulae were tolerated well by the sheep. Volume of effluent produced during the 60- to 120-hour period of diversion ranged from 7.7 to 14.9 L and tended to be greatest during the first 24 hours. All sheep became dehydrated, with mean PCV and plasma total protein concentration increases of 94.2 and 61.7%, respectively. Plasma chloride concentration decreased in linear fashion from a prediversion mean of 113 mEq/L (range, 111 to 117 mEq/L) to an end-point mean of 54 mEq/L (range, 45 to 65 mEq/L). Plasma sodium and potassium concentrations also decreased, though potassium concentration increased terminally. There were rapid increases in arterial blood pH and bicarbonate and base excess concentrations during the first 48 hours after diversion. However, during the final stages of diversion, sheep developed superimposed metabolic acidosis with increased plasma lactate concentration and high anion gap.

Abomasum↗

Renal net acid and electrolyte excretion in an experimental model of hypochloremic metabolic alkalosis in sheep.

Renal electrolyte and net acid excretion were characterized during generation and maintenance of hypochloremic metabolic alkalosis in a ruminant model. Two phases of renal response with regard to sodium and net acid excretion were documented. An initial decrease in net acid excretion was attributable to increase in bicarbonate excretion with associated increase in sodium excretion. As the metabolic disturbance became more advanced, a second phase of renal excretion was observed in which sodium and bicarbonate excretion were markedly decreased, leading to increase in net acid excretion and development of aciduria. Throughout the metabolic disturbance, chloride excretion was markedly decreased; potassium excretion also decreased. These changes were accompanied by increase in plasma renin and aldosterone concentrations. There was apparent failure to concentrate the urine optimally during the course of the metabolic disturbance, despite increasing plasma concentration of antidiuretic hormone.

Aldosterone↗

[Water-electrolyte and acid-base imbalance. IX. Respiratory alkalosis].

Respiratory alkalosis is the consequence of primary hypocapnia of divergent etiologies. Any pathologic process that increases ventilation to levels beyond that required to excrete the CO2 byproduct of metabolism, will result in an inappropriately low systemic pCO2 and a tendency to an alkaline systemic pH. The increased drive to ventilation may be due predominantly to a primary increase in central nervous system activity, either within the respiratory center itself or from more centrally placed areas with neural projections that extend to and control the respiratory center. Alternatively, an increased drive to ventilation may result from an "appropriate" physiologic response to another more important stimulus that overrides the human's needs to protect pCO2 and pH. Hypoxia (of different causes), is the most important and most commonly encountered such stimulus.

Alkalosis, Respiratory↗

[Metabolic alkalosis. III. Spontaneous and experimental compensation mechanisms in plasma and erythrocytes].

Plasma and red cell acid-base balance were studied in 13 patients with metabolic alkalosis and 14 healthy subjects following the infusion of bicarbonate. Differences between the plasma and red cell patterns suggested that application of the results of plasma determinations to the body as a whole could be the cause of serious inaccuracies. Since the changes noted occurred in different combinations according to whether alkalinisation was acute or not, it is felt that cell response to a fall in (H+) varies in relation to the time available for compensation.

Acid-Base Equilibrium↗

[Metabolic alkalosis. Compensation mechanisms in the light of new experimental data].

Changes in arterial blood and erythrocyte acid-base and electrolyte balance in the course of acute alkalinisation caused by bicarbonate loading showed that extracellular alkalosis has no significant effect on the concentration of intraerythrocyte bicarbonate concentration, though a marked increase in pH and electrolyte balance within the red cell is apparent. Erythrocyte alkalinisation may thus be seen as essentially due to the escape of H+ ions, while the entry of Na+ ions is the main device by which the law of electroneutrality is respected. The literature suggests that lactic acid offers a source of H+ ions for destruction of bicarbonate, whereas the diffusion of the ion lactate within the cell is compensated by the release of Cl-. In addition, the data now reported indicate that the red cell is a sufficiently valid model for the study of phenomena occurring within the intracellular compartment when a state of extracellular alkalinisation in created.

Aged↗

[Effects of acidosis and alkalosis on the sarcoplasmic reticulum of the heart].

Some functions of dog cardiac sarcoplasmic reticulum have been studied in acidosis and alkalosis conditions in a range of pH from 6.0 to 7.8. Intravesicular water content at pH 6.0 is 4.7 microliter per mg of protein and diminished to 4 microliter, (15%) at pH 8.0; this correlates with a drop of 13.5% in turbidity. Ca2+-dependent ATPase has an optimal pH of 7.2 and a specific activity of 580 nanomoles of ATP hydrolyzed/min/mg protein. The activity of Basal ATPase or Mg2+-dependent is insensitive to changes of pH. Maximal calcium uptake attains 45.1 +/- 1.4 nanomoles per mg protein between pH 6.0 and 6.6. The accumulated calcium diminished progressively when pH was raised. The rate of calcium transport in steady state shows an optimal pH of 6.7. The calcium transport kinetics constants shows that reticulum has a maximal affinity for calcium between pH 6.87 and 7.02. The maximal velocity for transport diminished progressively between pH 6.1 to 7.16. During the calcium transport process pH is changed from acid to alkaline and the accumulated calcium is release proportionally to the pH increment. This effect shows to be reversible. Calcium accumulation and ATP hydrolysis are uncoupled at pH values higher than 6.6 because to the increase in the rate of calcium release. Values of pK and number of protons per mg of protein that dissociates from ionizable residues are 6.53 and 0.68 respectively for calcium dependent ATPase; 7.09 and 0.60 for calcium transport and 7.41 and 0.39 for calcium release. We conclude that the rate of transport and affinity of cardiac sarcoplasmic reticulum for calcium are optimal between pH 6.8 and 7.0 that is the reported range of intracellular pH of normal cardiac tissue. The data are in close agreement with the fall of contractility in acidosis. It is proposed a calcium release pathway sensitive to pH and different from that of calcium pump, exclusively for entrance.

Acidosis↗

The effect of alkalosis on the glucose-mediated insulin release by the rat.

Bicarbonate loaded (alkalotic) rats had reduced plasma phosphate and ionized Ca concentrations and increased urinary cAMP excretion, phosphate clearance and pancreatic tissue uptake of extracellular calcium, all known effects of increased parathyroid hormone (PTH) secretion. Total insulin secretion after glucose challenge was enhanced in these animals. The response of alkalotic thyroparathyroidectomized rats, on the other hand, suggested exhaustion or inhibition of insulin secretion. The hypothesis is advanced that PTH, enhancing the permeability to calcium of the beta-cell membrane, compensated the effect of decreased calcium concentration in the extracellular fluid caused by alkalosis. PTH appears instrumental for homeostatic adjustments of insulin secretion.

Alkalosis↗

Necrotic skin lesion following therapy of severe metabolic alkalosis. A case report.

An outward side effect of HCl infusion during the treatment of severe metabolic alkalosis is reported. Solution of 0.2 n hydrochloric acid, infused via a peripheral vein caused necrotic lesions of skin and subcutaneous tissue. In case that the central parenteral route is precluded, oral therapy with diluted HCl solution may be considered.

Alkalosis↗

Influence of respiratory acidosis and alkalosis on volume of distribution of theophylline in dogs.

The volume of distribution of theophylline at nomal pH, and following induction of respiratory acidosis and alkalosis, was studied in four dogs in a three-way crossover design. Although serum half-lives of theophylline varied widely, and acidemia prolonged the time required for distribution equilibration, the volumes of distribution were almost identical for each of the three experimental conditions assuming one compartment pharmacokinetics apply.

Acidosis, Respiratory↗

[Hypokalemic alkalosis in patients with pyloroduodenal stenosis].

The work presents an analysis of results of examinations and treatment of 56 patients with Darrow hypokalemic alkalosis resulting from stenosis of the pylorus. In 45 of them the stenosis was caused by ulcer disease of the stomach and duodenum. The timely diagnosis, admission to the hospital and adequate therapy in 53 patients facilitated successful surgical interventions. In 3 patients the therapy was ineffective.

Adolescent↗

The syndrome of juxtaglomerular hyperplasia with aldosteronism, hypokalemic alkalosis and normal blood pressure.

In the syndrome of hypokalemic alkalosis, aldosteronism, elevated plasma renin and normal blood pressure, the juxtaglomerular apparatus shows hypertrophy and hyperplasia of all elements. Renal handling of sodium is abnormal: despite excessive delivery of proximal fluid to distal sites so that potassium secretion is excessive, free water formation is subnormal. The syndrome is frequently familial, but no inherited case is known. In erythrocytes low sodium efflux coefficient and high sodium concentration may serve as "markers" for the syndrome. In two cases, products of consanguineous relations, autosomal recessive inheritance is suggested.

Alkalosis↗

[Recurrent metabolic alkalosis due to pyloric stenosis].

After an inability to work lasting 15 months with 9 treatments in an inpatient department in several institutions in a 33-year-old patient the relapsing metabolic alkalosis in hypopotassiaemia and relapsing increase of the creatinine level could causally be clarified by establishment of a pylorus stenosis in chronic duodenal ulcer. Due to the Billroth II operation a complete clinical and objective improvement developed. In this case the transient retention of substances normally contained in the urine was conditioned by a hypokalaemic nephropathy. The cause of the hypokalaemia was the vomiting by pylorus stenosis. The histologically ascertained glomerulonephritis had no causal significance for the pathological process.

Adult↗

Excretion of ammonia by rat kidney during metabolic alkalosis.

In rat kidney, proximal tubular and final urinary ammonia concentration are finite. They are lower in animals with metabolic alkalosis than in controls. A positive correlation between ammonia concentration and water removal (as indicated by fluid to plasma ratios for inulin) was found. A comparison of tubular fluid to plasma concentration ratios for inulin and ammonia indicates that more ammonia enters proximal tubular fluid than appears in the final urine. These observations indicate that ammonia is probably secreted primarily at the level of the proximal tubule and then undergoes reabsorption at distal sites of the nephron.

Alkalosis↗

Changes in renal handling of platinum in cisplatinum-treated rats following induction of metabolic acidosis or alkalosis.

Manipulations of metabolic acid-base status were used in an attempt to modify the renal handling and toxicity of the anticancer drug cisplatinum. Rats were orally pretreated with either tap water (TW), ammonium chloride (AC), or sodium bicarbonate (SB) for 3 days prior to intraperitoneal administration of a high cisplatinum dose (7.5 mg/kg b.w.). Urine was collected daily for 4 days between drug dosing and killing of the animals. AC-pretreated rats did not exhibit the characteristic cisplatinum-induced diuresis and were unable to maintain an acid urinary pH following drug administration. AC rats had a significantly lower, and SB rats a significantly higher, urinary excretion of platinum than did TW rats. Platinum excretion was found to be correlated with urinary pH (r = 0.88) and not urinary volume (r = 0.30). The renal concentration of platinum was greater in AC animals than in SB or TW animals, but no significant difference was observed in liver or plasma concentrations between the groups. Both pretreated groups had equal percent of free vs bound platinum. Proteinuria was more severe in AC-pretreated rats, but histologic evidence of renal tubular damage was present in all the three groups. It is concluded that metabolic acidosis can seriously impair the renal handling of high dose cisplatinum but that metabolic alkalosis offers no evident advantages over nonpretreatment.

Acid Phosphatase↗

Metabolic alkalosis secondary to baking soda treatment of a diaper rash.

A 4-month-old infant was seen with hypokalemic metabolic alkalosis that was associated with prior application of liberal amounts of sodium bicarbonate (baking soda) to a diaper rash. After exclusion of other etiologies of the infant's acid-base disturbance, a complete resolution occurred following discontinuation of the baking soda applications. This case report provides a reminder of the significant side effects that may result from the excessive use of a seemingly harmless household substance.

Alkalosis↗