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PubMed1987

Parallel adaptation of the rabbit renal cortical sodium/proton antiporter and sodium/bicarbonate cotransporter in metabolic acidosis and alkalosis.

Recent studies have shown that the bicarbonate reabsorptive capacity of the proximal tubule is increased in metabolic acidosis. For net bicarbonate reabsorption to be regulated, there may be changes in the rate of apical H+ secretion as well as in the basolateral base exit step. The present studies examined the rate of Na+/H+ exchange (acridine orange method) and Na+/HCO3 cotransport (22Na uptake) in apical and basolateral membranes prepared from the rabbit renal cortex by sucrose density gradient centrifugation. NH4Cl loading was used to produce acidosis (arterial pH, 7.27 +/- 0.03), and Cl-deficient diet with furosemide was used to produce alkalosis (arterial pH, 7.51 +/- 0.02). Maximal transport rate (Vmax) of Na+/H+ antiporter and Na+/HCO3 cotransporter were inversely related with plasma bicarbonate concentration from 6 to 39 mM. Furthermore, the maximal transport rates of both systems varied in parallel; when Vmax for the Na+/HCO3 cotransporter was plotted against Vmax for the Na+/H+ antiporter for each of the 24 groups of rabbits, the regression coefficient (r) was 0.648 (P less than 0.001). There was no effect of acidosis or alkalosis on affinity for Na+ of either transporter. We conclude that both apical and basolateral H+/HCO3 transporters adapt during acid-base disturbances, and that the maximal transport rates of both systems vary in parallel during such acid-base perturbations.

Acidosis↗
PubMed1991

Bicarbonate secretion in vivo by rat distal tubules during alkalosis induced by dietary chloride restriction and alkali loading.

To examine in vivo the separate effects on distal tubule JtCO2, of dietary chloride restriction, bicarbonate loading, and changes in luminal chloride concentration, we microperfused distal tubules at a physiologic flow rate (8 nl/min) with solutions containing either 45 or 0 mM chloride (after gluconate substitution). Rats were fed a diet containing zero, minimal, or normal amounts of chloride, while drinking either water or a solution of 0.15 M sodium bicarbonate. Neither extracellular fluid volume contraction nor negative chloride balance ensued. Analysis of covariance with repeated measures demonstrated that dietary chloride, drinking sodium bicarbonate, and perfusion with either 45 mM or zero chloride, each have separate and significant modulating effects on distal tubule bicarbonate secretion. During mild alkalemia, there is modest bicarbonate secretion which is significantly different from zero (-9.9 +/- 3.2 pmol.min-1.mm-1, P less than 0.01), and which is suppressed after perfusion with zero chloride. In contrast, during more pronounced metabolic alkalosis after supplemental bicarbonate drinking, the bicarbonate secretory flux is brisk (-26 +/- 3 pmol.min-1.mm-1) and significantly different from zero and persists (-11 +/- 3 pmol.min-1.mm-1) even during perfusion with zero luminal chloride. Accordingly, in this two-day model of alkalosis induced by dietary chloride restriction, there is regulatory secretion of bicarbonate by distal tubules in vivo which is modulated by luminal chloride concentration.

Absorption↗
PubMed2001

The lactic acid response to alkalosis in panic disorder : an integrative review.

Panic patients consistently show exaggerated lactic acid response to alkalosis, whether produced by hyperventilation or by sodium lactate infusion. Understanding why this occurs may provide important clues to the pathogenesis of panic disorder. Although brain hypoxia from excessive hypocapnia-induced cerebral vasoconstriction is often cited as the mechanism of elevated brain lactic acid in panic disorder, studies of brain metabolism show that hypocapnia rarely leads to brain hypoxia. Increased lactic acid production is a normal response to intracellular alkalosis and to intracellular cyclic AMP. Thus, other possible mechanisms of the exaggerated lactic acid response in panic disorder include a disturbance of mechanisms regulating intracellular pH and factors increasing intracellular cyclic AMP. Both mechanisms are consistent with the suffocation false alarm theory of panic disorder. This review suggests a theoretical framework for future magnetic resonance spectroscopy studies that can test some of the predictions of these competing models.

Alkalosis↗
PubMed2005

Alkalosis and the plasma catecholamine response to high-intensity exercise in man.

PURPOSE: The aims of this study were to examine the plasma dopamine response to a controlled bout of short-duration high-intensity exercise and investigate the magnitude of the plasma dopamine (DA), norepinephrine (NE), and epinephrine (EPI) responses to this exercise after induced alkalosis. METHODS: Eight male subjects were given in randomized order either; PLAC 0.3 g.kg(-1) body mass CaCO3 + 1 g NaCl, 0.3CIT 0.3 g.kg(-1) or 0.5CIT 0.5 g.kg(-1) body mass tri-sodium citrate in 500 mL water. One hour after ingestion subjects performed a 2-min cycle test at a workload calculated to elicit 110% VO(2max). Plasma catecholamines were measured using high performance liquid chromatography with electrochemical detection. RESULTS: Antecubital venous blood pH and blood base excess (BBE) were significantly increased after ingestion of sodium citrate compared with placebo (P < 0.05). All postexercise sodium citrate blood pH and BBE values were significantly greater than placebo (P < 0.05). High-intensity exercise did not affect resting plasma DA concentrations. Peak plasma NE and EPI concentrations occurred immediately postexercise [NE PLAC 4.6 +/- 2.1 ES = 1.2, 0.3CIT 4.2 +/- 1.8 ES = 1.5, 0.5CIT 4.6 +/- 2.2 nmol.L(-1) ES = 1.2; EPI PLAC 0.6 +/- 0.3 ES = 1.3, 0.3CIT 0.5 +/- 0.2 ES = 1.3, 0.5CIT 0.5 +/- 0.3 nmol.L(-1) ES = 0.8] and were still elevated 5 min postexercise (P < 0.05). The magnitude of the plasma dopamine, norepinephrine and epinephrine response to exercise was unaltered with either 0.3CIT or 0.5CIT. CONCLUSION: This study has demonstrated that performance of a controlled bout of high-intensity exercise did not alter the plasma dopamine concentration. In addition, alterations in blood alkalosis did not influence the magnitude of the plasma dopamine, norepinephrine or epinephrine responses to exercise.

Acid-Base Equilibrium↗
PubMed1997

Metabolic alkalosis in coliform mastitis.

Values of blood gas, serum chloride, and potassium were tabulated for 21 dairy cows with coliform mastitis. Severe cases showed marked clinical signs such as loss of appetite and depression of digestive tract motility, and metabolic alkalosis such as an increase in blood pH, hypochloremia and hypokalemia compared with normal and mild cases (p < 0.01). The results showed that metabolic alkalosis can be detected more easily than acidosis in cases of severe coliform mastitis.

Alkalosis↗
PubMed1996

Metabolic alkalosis and myoclonus from antacid ingestion.

A patient with a history of cerebrovascular disease, hypertension, and previous gastrectomy developed metabolic alkalosis and myoclonus. His medications included the anti-hypertensive agents nicardipine hydrochloride, delapril, prazosin; dihydroergotoxin and ticlopidine for cerebral infarction; estazolam for insomnia; azuren-L-glutamine compound and S-M powder. In addition, he had taken 12 grams per day of Ohta's Isan antacid, which contained 625 mg sodium bicarbonate per 1.3 g of antacid powder over a 6-month period. This antacid is commonly used in Japan. This is the first report of a case of metabolic alkalosis and myoclonus secondary to ingestion of a commercially available antacid in Japan.

Aged↗
PubMed1975

Gout as a complication of Bartter's syndrome. A possible role for alkalosis in the decreased clearance of uric acid.

A prevalence of hyperuricemia of 50% and of acute gouty arthritis of 20% has been observed in a group of patients with Bartter's syndrome. All patients except one presented initially with complaints unrelated to uric acid metabolism. The cause of their hyperuricemia and subnormal clearance of uric acid is unexplained. Systemic alkalosis, a prominent feature of Bartter's syndrome, can decrease the clearance of uric acid and may contribute to the hyperuricemia and gout that have been observed. Physicians should be aware of the possibility of gout as a clinical complication of Bartter's syndrome and of the inhibitory effects of alkalosis on urate clearance.

Acute Disease↗
PubMed1977

Correction of postoperative metabolic alkalosis and renal failure by hemodialysis.

Three postoperative patients with oliguirc renal failure and hypochloremic metabolic alkalosis were treated with hemodialysis using a specailly prepared high-chloride, low-acetate dialysate. This mode of therapy corrected the metabolic abnormalities and was significantly more effective than treatment with commercially available high-acetate dialysate at increasing the serum chloride and hydrogen ion concentration. Furthermore, hemodialysis with high-chloride, low-acetate dialysate corrected the clinical sequelae of hypoventilation, cardiac arrhythmia, and neuromuscular irritability associated with metabolic alkalosis while treating uremia simultaneously.

Acute Kidney Injury↗
PubMed2000

Penumbral tissue alkalosis in focal cerebral ischemia: relationship to energy metabolism, blood flow, and steady potential.

The effect of focal ischemia on tissue pH was studied at various times up to 6 hours after permanent middle cerebral artery occlusion in rats. Tissue pH was imaged by using umbelliferone fluorescence and correlated with cerebral blood flow, ATP content, and recordings of the steady potential. Circumscribed foci of allalosis (pH 7.32+/-0.11) were detected with increasing frequency in penumbral regions having near-to-normal ATP concentrations and cerebral blood flow values between 20% and 40% of control. Both the infarct core, defined by ATP loss and cerebral blood flow values of less than 20% of control, and the inner peri-infarct rim were consistently acidic (pH 6.03+/-0.36 and 6.53+/-0.24, respectively). Treatment with the glutamate antagonist dizocilpine (MK-801) suppressed negative shifts of the steady potential and reduced significantly the occurrence of alkalosis observed in 90% of untreated but only in 44% of treated animals. Penumbral alkalosis appeared to be a time-dependent event occurring 30 to 60 minutes after the passage of peri-infarct depolarizations. The diversity of penumbral pH changes reflects the local disturbance of pH regulation and, possibly, the differential fate of penumbral subareas.

Acidosis↗
PubMed2001

Hypokalemic metabolic alkalosis--three case reports.

The two most common forms of inherited normotensive hypokalemic metabolic alkalosis are Bartter's and Gitelman's syndromes. Bartter's syndrome typically present with normal or increased calcium excretion. Hypomagnesemia occurs in only one third of affected individuals. In contrast, hypomagnesemia and hypocalciuria are considered hallmarks of Gitelman's syndrome. In most patients, the symptom of muscle weakness and polyuria occur early in life, which may be attributed to potassium depletion. Despite hyperaldosteronism, the patients tend to be normotensive, which is at least explained by vascular hyperresponsiveness to prostaglandins. Therapeutic approaches to Bartter's and Gitelman's syndromes include potassium supplementation, prostaglandin synthesis inhibitors (nonsteroid anti-inflammatory agents), aldosterone antagonists and converting enzyme inhibitors. Three patients with hypokalemia, normal blood pressure, metabolic alkalosis, hyperreninemia and hyperaldosteronism are described. Two patients had Bartter's syndrome and one patients had Gitelman's syndrome.

Adult↗
PubMedDate not supplied

[Redox processes in the retina and tunic tissues of the rat eye in experimental alkalosis].

It is shown in experiments is vivo that development of experimental metabolic alkalosis in rats is followed by changes in redox processes in the eye retina and tunic. For the first two months of the experiment the number of sulphydryl group decreases, while that of disulphide ones of water-soluble proteins and low-molecular compounds increases. The amount of oxidized metabolites of glycolysis and of a cycle of tricarboxylic acids (pyruvate, oxaloacetate, alpha-ketoglutarate) increases relative to the reduced ones (lactate, isocitrate, malate), as well as activities of hexokinase, pyruvate kinase, NAD-dependent malate dehydrogenase, while activities of fructose diphosphatase, glucoso-6-phosphate dehydrogenase, glutathione peroxidase and glutathione reductase fall. The content of malonic dialdehyde increases. 90 days later disorders of certain compensatory mechanisms of the metabolic system of alkalosis regulation probably occurred in the eye retina and tunic tissues: hexokinase and pyruvate kinase activity fell to the control values, while that of NAD-dependent malate dehydrogenase--below the control level; the content of lactate increased. Activity of glutathione-dependent enzymes remained low and the amount of malonic dialdehyde grew much more than in the previous terms.

Alkalosis↗
PubMed1992

[Excretion of urea and ammonia and its effect on the acid-base balance of water in the habitat of the anuran amphibian Xenopus laevis. Action of metabolic alkalosis].

We studied in Xenopus laevis the effect of changing the salinity and the acid-base status of the ambient water on the total nitrogen catabolism and the nature of the nitrogen end products, urea and ammonia. Increase of the ambient osmolarity by addition of NaCl led to a rise in protein catabolism and to a predominant ureotelism which can approach 95% of the excreted nitrogen. The osmolarity can reach 500 mosmol. L-1 without obvious harmful effects. NaCl can then be replaced by NaHCO3 without injury to the animal as long as water alkalosis is avoided by an appropriate increase of the ambient CO2 tension, PCO2. However, if PCO2 is kept low, the resulting water metabolic alkalosis causes death within a few hours.

Acid-Base Equilibrium↗
PubMed2005

[Serious postoperative metabolic alkalosis during hospitalization].

Metabolic alkalosis is a frequent and serious abnormal acid-base disturbance with a high-pH-dependent morbidity and mortality rate. This situation is easy to recognize, and the treatment is relatively simple. We present a case history dealing with metabolic alkalosis as a consequence of severe acid-base disturbance with electrolyte and fluid imbalance caused by continuous postoperative vomiting and nasogastric suction. Our aim is to attract greater attention to this acid-base disturbance and a better understanding of the pathogenesis, which in turn should lead to earlier intervention and more appropriate therapy.

Alkalosis↗
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↗
PubMed1991

[The course of rumen fermentation during alkalosis in cows].

The aim of the study was the investigation of rumen fermentation during alkalosis in cows. The study comprised some parameters of rumen fermentation, such as: pH, ammonia and volatile fatty acids (VFA) levels, also relationship between VFA, numbers of population of protozoa and bacteria, total production of gases in vitro particularly CO2 and CH4, amounts of lactic and total protein in rumen fluid and non-glucogenic/glucogenic ratio (NGGR) in the VFA mixture. On the basis of obtained results the amounts of fermented hexose, cell yield, ATP produced and hydrogen utilization were calculated. During alkalosis there was observed significant fall of VFA production, especially acetic and butyric acids, also lower production of gases, particularly CH4--probably as a result of selective reduction of methanogenic strain bacteria. The levelling of value of rumen pattern of fermentation occurred after the beginning of lactation probably as a result of metabolism products excretion together with milk.

Acetates↗
PubMed1991

Acetazolamide in the treatment of metabolic alkalosis in critically ill patients.

Metabolic alkalosis is a common acid-base disturbance in critically ill patients. In many patients correction of fluid and electrolyte status does not fully correct the metabolic derangement. In this study we examined the effect of 500 mg of intravenous acetazolamide, after correcting for fluid and electrolyte abnormalities, on the acid-base status of 30 ventilated patients. In all patients studied there was a fall of total serum bicarbonate; the mean reduction at 24 hours was 6.4 mmol/L, with a normalization of the base excess and pH. The onset of action was rapid (within 2 hours), and the maximal effect occurred at a mean of 15.5 hours, although there was wide variation. The effect of acetazolamide was still apparent at 48 hours. No adverse effects were noted. We conclude that in patients with metabolic alkalosis, once fluid and electrolyte abnormalities have been corrected, acetazolamide is an effective and safe form of therapy with a quick onset and long duration of action.

Acetazolamide↗
PubMed1975

[Nature of metabolic alkalosis in the postoperative period in patients with pulmonary tuberculosis].

Sixty five patients with pulmonary tuberculosis subjected to extensive and traumatic surgical interventions were investigated. Metabolic alkalosis to the end of the 1st--2d postoperative day would develop in patients, who showed acid-base balance disorders toward acid aspect during the operation. In the mechanism of development of a grave decompensated postoperative metabolic alkalosis the role of a trigger factor is played by a massive intraoperative blood loss with marked hemodynamic disturbances in the immediate postoperative period.

Acid-Base Equilibrium↗
PubMed1975

Paradoxic aciduria in bovine metabolic alkalosis.

Cows with metabolic alkalosis secondary to abomasal displacement and other abomasal disorders were often found to excrete acidic urine. This paradoxic aciduria contradictsthe classical view that the pH of the urine may be used to estimate the acid-base status of the body. Data from bovine clinical patients with metabolic alkalosis, serum electrolyte changes, and paradoxic aciduria suggested that the balance of sodium potassium, and chloride in the body places limits on the kidneys' ability to regulate the acid-basebalance.

Abomasum↗