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PubMed1992

Chronic neutral phosphate supplementation induces sustained, renal metabolic alkalosis.

The aim of the present study was to test whether intravenous neutral phosphate supplementation, recently shown in our laboratory to acutely stimulate proton secretion in the distal nephron, was able to induce a sustained metabolic alkalosis. Neutral Na and K phosphate supplementation for seven days, with equivalent reduction in chloride supply and unchanged intake of sodium and potassium, in ADX rats receiving fixed physiological doses of aldosterone and dexamethasone (group 1, N = 7), was responsible for a severe metabolic alkalosis (MA; delta [HCO3] 11 +/- 1.3 mM, and delta pH 0.11 +/- 0.06 unit). Metabolic alkalosis was at least in part of renal origin, since net acid excretion (NAE) transiently increased, principally due to an increment in titratable acid excretion rate. Balances were equilibrated for sodium and negative for chloride and potassium, which may have contributed to the severity of the MA. Chronic i.v. neutral Na phosphate, without change in potassium and chloride supply, in ADX rats receiving the same doses of steroids (group 2, N = 5), was responsible for a less severe MA (delta [HCO3] 7.5 +/- 0.9 mM, and delta pH 0.07 +/- 0.01 unit), also of renal origin. In this group, balances were positive for chloride and sodium and equilibrated for potassium. Finally, neutral Na and K phosphate supplementation with reduction in chloride supply in intact rats (group 3, N = 4) was also able to induce a MA (delta [HCO3] 5.5 +/- 1.8 mM, and delta pH 0.06 +/- 0.01 unit) of renal origin, with balances negative for chloride and equilibrated for potassium and sodium. In all groups, the generation and maintenance of MA probably resulted from stimulated proton secretion in the distal nephron, as suggested by the observed increase of PCO2 over HCO3 concentration ratio in the urine and a fall in urine pH despite augmented urinary buffer content throughout the phosphate infusion period. Glomerular filtration rate did not significantly vary in any group. In conclusion, chronic supplementation of neutral phosphate appears to stimulate per se proton secretion in the distal nephron, independently of sodium, chloride, and potassium balances, and adrenal steroid secretion. Thus neutral phosphate supplementation should be added to the previously known factors able to induce MA.

Acid-Base Equilibrium↗
PubMed1977

Effects of metabolic alkalosis, metabolic acidosis and uraemia on whole-body intracellular pH in man.

1. Whole-body intracellular pH (pHi) was measured by the 14C-labelled DMO method in twenty-four control subjects, eighteen normal subjects with induced acute metabolic alkalosis, ten normal subjects with induced acute metabolic acidosis, twelve normal subjects with chronic acidosis and in fifteen patients with chronic renal insufficiency and acidosis. 2. The change in pHi per unit change in extracellular pH is significantly larger in acute metabolic alkalosis than in acute metabolic acidosis. In chronic metabolic acidosis, pHi decreased in proportion to the total amount of ammonium chloride administered; pHi was normal in patients with uraemic acidosis. 3. These observations confirm the role that tissue buffers play in the protection of the cellular environment in some forms of acidosis. When the acid load overwhelms tissue buffer capacity, pHi becomes a function of extracellular pH. 4. Cells seem more protected from acute acidosis than from acute alkalosis.

Acid-Base Equilibrium↗
PubMed1983

Development of the respiratory compensation to progressive metabolic alkalosis resulting from potassium depletion in conscious rats.

1. 288 arterial blood samples were obtained at successive times, through indwelling catheters, from conscious rats subjected to selective dietary potassium restriction for up to 5 weeks. 2. In control rats with unrestricted access to potassium [HCO-3]a = 25.4 mmol/l, pHa = 7.47, PaCO2 = 34 mmHg, PaO2 = 94 mmHg and [K+]a = 4.3 mmol/l were steady and within the range of values reported in conscious rats. Five weeks of isolated potassium restriction resulted in significant hypokalaemia ([K+]a = 2.15 mmol/l) and metabolic alkalosis ([HCO-3]a = 34.1 mmol/1, pH 7.57). This alkalosis, due mostly to H+ transfer into cells, was accompanied by a significant increase in PaCO2 to 36.4 mmHg and decrease in PaO2 to 88 mmHg, contrary to previous reports in man and dog. The administration of neutral sodium phosphate in addition to potassium restriction enhanced both the alkalosis ([HCO-3]a = 42.3 mmol/l, pH 7.61) and its respiratory compensation (PaCO2 = 40.8, PaO2 = 82 mmHg), without altering the PaCO2: [HCO-3]a relationship. 3. The opposite variations of PaCO2 and PaO2 were significantly correlated to the increase in plasma bicarbonate concentration and described best by crossed sigmoid curves. The equations of both curves were calculated; their point of inflection occurred at the same bicarbonate concentration (36 mmol/l). The maximum intensity of respiratory compensation (0.62 mmHg PaCO2 for each mmol [HCO-3]a/l) observed at this point fell within the range of values yielded by previous estimations.

Alkalosis↗
PubMed1990

No effect of bicarbonate-induced alkalosis on urea synthesis in normal man.

The effect of metabolic alkalosis was studied in 10 healthy volunteers. In each person urea synthesis was determined in two periods of 2 h as urinary excretion corrected for accumulation in body water and for intestinal hydrolysis. Infusion of bicarbonate (115 mmol/h) increased pH of the venous blood by 0.10 units. In four subjects fasting urea synthesis was 24 mmol N/h at normal pH and unaffected by alkalosis (mean difference +/- SED was 1.04 +/- 4.1). In six subjects alanine was infused so as to increase blood alanine concentration from 0.4 to 2.5 mmol/l and urea synthesis to 107 mmol N/h. Alkalosis did not change urea synthesis (mean difference +/- SED was 1.5 +/- 7.4 mmol N/h). The results favour the view that urea synthesis mainly serves to eliminate nitrogen, but do not support the hypothesis that urea synthesis is an important immediate and direct regulatory process in acute acid-base disturbances.

Adult↗
PubMed2006

TRPC4 expression determines sensitivity of the platelet-type capacitative Ca2+ entry channel to intracellular alkalosis.

The present study was designed to analyze the molecular basis of the intracellular pH-dependent capacitative Ca2+ entry (CCE) of human platelets and megakaryocytic cells, specifically to test the hypothesis that members of the classical transient receptor potential (TRPC) protein family are involved in the CCE pathway that is promoted by intracellular alkalosis. Human platelets as well as the tested megakaryocytic cell lines (CMK cells, MEG-01 cells) and HEK293 cells displayed thapsigargin-induced CCE and responded to monensin with comparable elevation in intracellular pH. Promotion of CCE by monensin-induced intracellular alkalosis, however, was profound in mature platelets, moderate in CMK cells and lacking in MEG-01 cells as well as in HEK293 cells. Analysis of the TRPC expression pattern by immunoblotting revealed that mature platelets and CMK cells express TRPC4 along with TRPC1 and TRPC3, while TRPC4 is lacking in MEG-01 cells. HEK293 cells displayed CCE characteristics as well as lack of TRPC4 expression similar to MEG-01 cells. Over-expression of TRPC4 in HEK293 cells was found to result in a gain of pH-sensitivity of CCE with clearly detectable promotion of CCE in response to monensin. These results suggest that platelet CCE channel complexes contain TRPC4 as a molecular component that determines sensitivity of CCE to intracellular alkalosis.

Alkalosis↗
PubMed1986

Tetany induced by hypokalemia in the absence of alkalosis.

A 36-year-old patient developed tetany manifested only by a positive Trousseau's sign and with a negative Chvostek's sign 8 weeks after gastric bypass surgery for obesity. The usual causes of tetany (hypocalcemia, hypomagnesemia and alkalosis) were absent. The only possible etiology found was hypokalemia. Previous cases of hypokalemia induced tetany reported were always accompanied by alkalosis. Its absence in our patient makes this case unique and determines that hypokalemia per se in the absence of alkalosis may be a cause of tetany. It is suggested that the Trousseau's sign should be investigated in patients with severe potassium deficiency.

Adult↗
PubMed1997

The effects of bupivacaine and ropivacaine on baroreflex sensitivity with or without respiratory acidosis and alkalosis in rats.

Systemic toxicity of local anesthetics causes cardiac and central nervous system (CNS) depression that could be enhanced in the presence of respiratory acidosis. We examined a potential suppression of baroreflex function with bupivacaine and ropivacaine during hypercapnic acidosis or hypocapnic alkalosis. Baroreflex sensitivity (BRS) was randomly tested in rats with one of 13 conditions during intravenous administration of saline (control), bupivacaine 1, 2, or 3 mg/kg, or ropivacaine 2, 4, or 6 mg/kg. The effects of bupivacaine (3 mg/kg) or ropivacaine (6 mg/kg) on BRS were also examined during hypercapnic acidosis or hypocapnic alkalosis. The BRS was assessed using a value of delta heart rate/ delta mean arterial pressure after infusion of phenylephrine (3 micrograms/kg). Both bupivacaine and ropivacaine (at the largest dose) significantly suppressed BRS. Acute respiratory acidosis (pHa 7.24 +/- 0.04, Paco2 63 +/- 4 mm Hg) enhanced BRS. The BRS enhanced during acidosis was also suppressed with bupivacaine and ropivacaine, but less so than in the absence of acidosis. The presence of hypocapnic alkalosis (pHa 7.55 +/- 0.03, Paco2 25 +/- 2 mm Hg) did not affect BRS and reversed BRS suppression caused by both drugs. Thus, bupivacaine and ropivacaine affect neuronal control mechanisms for maintaining cardiovascular stability, and acute changes of respiration could significantly modify such suppression.

Acidosis, Respiratory↗
PubMed1987

Development of metabolic alkalosis after massive transfusion during orthotopic liver transplantation.

Five patients undergoing orthotopic liver transplantation were investigated for changes in acid-base homeostasis secondary to large volume transfusions. All patients developed a transient acidemia during the operative period, followed by alkalemia which persisted into the early postoperative period. The patients received an estimated mean of 750 mEq of citrate, which appeared to cause metabolic alkalosis. The biochemical basis underlying the regulation of citrate metabolism that may have led to the timing, extent, and duration of the subsequent metabolic alkalosis is presented. Finally, the time course for the development of metabolic alkalosis may be a potentially sensitive indicator of early allograft function.

Acid-Base Imbalance↗
PubMed1979

Metabolic alkalosis complicating weaning from mechanical ventilation.

Metabolic alkalosis was identified and confirmed as a precipitator of acute hypercapnea. As a result, weaning from mechanical ventilator therapy was delayed. Correction of alkalosis followed by reduction of PCO2 confirmed the compensatory mechanism during alkalosis, and weaning from intermittent mandatory ventilation then proceeded at an appropriate rate.

Acetazolamide↗
PubMed1979

Treatment of metabolic alkalosis with intravenous hydrochloric acid.

Severe alkalosis requires aggressive treatment. Twenty patients at the Talmadge Memorial Hospital have been treated for metabolic alkalosis by infusion of dilute hydrochloric acid through a central venous line. The treatment was effective and there were no major complications. Intravenous hydrochloric acid is preferred to other modes of therapy for refractory alkalosis, especially in the presence of hepatic or renal failure.

Adolescent↗
PubMed1986

Marked hypochloremic metabolic alkalosis with severe compensatory hypoventilation.

In metabolic alkalosis, a compensatory decrease in alveolar ventilation with hypercapnia has been noted only rarely. We recently managed a patient with gastric outlet obstruction from a duodenal ulcer who survived after arriving in the emergency room comatose with severe hypochloremic metabolic alkalosis, compensatory hypoventilation, and hypercapnia. We know of no report in the English literature of a patient with gastric outlet obstruction having a respiratory acidosis or hypochloremia as severe as that in our patient. Proper understanding of the pathophysiology of primary metabolic alkalosis due to gastric losses is necessary to correct the acid-base abnormalities quickly and to restore normal alveolar ventilation.

Alkalosis↗
PubMed1983

Carbon dioxide elimination after acetazolamide in patients with chronic obstructive pulmonary disease and metabolic alkalosis.

Acetazolamide, an inhibitor of carbonic anhydrase, which catalyzes hydration/dehydration of carbon dioxide, has been used for correction of metabolic alkalosis in patients with chronic obstructive pulmonary disease (COPD). Animal experiments have shown that the gradient between tissue and the alveolar CO2 tension increases after inhibition of carbonic anhydrase, suggesting retention of CO2. In order to determine the true degree of carbon dioxide retention after total inhibition of carbonic anhydrase, 10 patients with COPD and pronounced metabolic alkalosis (base excess above 6) under controlled mechanical ventilation were studied. The study showed that there was a statistically significant increase in tissue PCO2 and a temporary decrease in pulmonary carbon dioxide excretion. Furthermore, it was found that PaO2 and PVO2 increased significantly after inhibition of carbonic anhydrase, which could, at least partly, explain the improvement seen in patients with COPD and metabolic alkalosis after treatment with acetazolamide.

Acetazolamide↗
PubMed1998

Na/H exchange and H-K ATPase increase distal tubule acidification in chronic alkalosis.

We examined whether H(+)-ATPase, H(+)-K(+)-ATPase, and or Na+/H+ exchange mediates increased distal tubule acidification in animals with chronic metabolic alkalosis using pharmacological inhibitors of these H+ transporters in in vivo-perfused tubules of anesthetized rats. Chronic metabolic alkalosis was induced with furosemide followed by minimum electrolyte diet and HCO3 drinking water. The reduction in net HCO3 reabsorption was greater in distal tubules of alkalotic compared to control animals perfused with Schering 28080 to inhibit H(+)-K(+)-ATPase (-6.4 +/- 0.9 vs. -1.4 +/- 0.5 pmol/mm.min-1, P < 0.02) and with EIPA to inhibit Na+/H+ exchange (-11.1 +/- 1.7 vs. -6.6 +/- 0.9 pmol/mm.min-1, P < 0.01) but was similar in distal tubules of alkalotic and control animals perfused with bafilomycin to inhibit H(+)-ATPase. The greater reduction of distal tubule net HCO3 reabsorption in alkalotic compared to control animals induced by EIPA was eliminated by systemic infusion of the endothelin receptor antagonist bosentan (-4.6 +/- 0.7 vs. -4.4 +/- 0.7 pmol/mm.min-1, P = NS) but the greater reduction induced by Schering 28080 persisted. Urine endothelin-1 (ET-1) excretion was higher in animals with maintained alkalosis (164.5 +/- 23.7 vs. 76.6 +/- 10.8 fmol/day, P < 0.03), but decreased following KCl repletion to a value (86.7 +/- 10.0 fmol/day, P < 0.02 vs. respective before-KCl value) that was not different from that for KCl-repleted control animals (79.9 +/- 8.7 fmol/day, P = NS vs. KCl-repleted alkalotic animals). The data support that augmented distal tubule acidification in alkalotic animals is due to increased H(+)-K(+)-ATPase and Na+/H+ exchange activity, the latter stimulated by endogenous endothelins.

Acid-Base Equilibrium↗
PubMedDate not supplied

Gastric conduit urinary diversion in normal dogs. Part II, Hypochloremic metabolic alkalosis.

Gastric conduit urinary diversion was performed in 10 dogs after complete cystectomy. Four dogs were euthanatized on day 30 because of hypochloremic metabolic alkalosis and renal failure. Hematologic and biochemical changes in six dogs evaluated for 120 days were compatible with hypochloremic metabolic alkalosis. The continuous loss of hydrochloric acid from the gastric conduit resulted in significant increases in arterial blood pH, PaCO2, anion gap, TCO2, and the concentration of HCO3-. There were significant decreases in PaO2 and the serum concentrations of chloride and potassium. Deterioration of renal function resulted in all dogs. It was concluded that hypochloremic metabolic alkalosis makes gastric conduit urinary diversion unsatisfactory for clinical use in dogs.

Acid-Base Equilibrium↗
PubMed2005

Alkalosis increases muscle K+ release, but lowers plasma [K+] and delays fatigue during dynamic forearm exercise.

Alkalosis enhances human exercise performance, and reduces K+ loss in contracting rat muscle. We investigated alkalosis effects on K+ regulation, ionic regulation and fatigue during intense exercise in nine untrained volunteers. Concentric finger flexions were conducted at 75% peak work rate (3 W) until fatigue, under alkalosis (Alk, NaHCO3, 0.3 g kg(-1)) and control (Con, CaCO3) conditions, 1 month apart in a randomised, double-blind, crossover design. Deep antecubital venous (v) and radial arterial (a) blood was drawn at rest, during exercise and recovery, to determine arterio-venous differences for electrolytes, fluid shifts, acid-base and gas exchange. Finger flexion exercise barely perturbed arterial plasma ions and acid-base status, but induced marked arterio-venous changes. Alk elevated [HCO3-] and PCO2, and lowered [H+] (P < 0.05). Time to fatigue increased substantially during Alk (25 +/- 8%, P < 0.05), whilst both [K+]a and [K+]v were reduced (P < 0.01) and [K+]a-v during exercise tended to be greater (P= 0.056, n= 8). Muscle K+ efflux at fatigue was greater in Alk (21.2+/- 7.6 micromol min(-1), 32 +/- 7%, P < 0.05, n= 6), but peak K+ uptake rate was elevated during recovery (15 +/- 7%, P < 0.05) suggesting increased muscle Na+,K+-ATPase activity. Alk induced greater [Na+]a, [Cl-]v, muscle Cl- influx and muscle lactate concentration ([Lac-]) efflux during exercise and recovery (P < 0.05). The lower circulating [K+] and greater muscle K+ uptake, Na+ delivery and Cl- uptake with Alk, are all consistent with preservation of membrane excitability during exercise. This suggests that lesser exercise-induced membrane depolarization may be an important mechanism underlying enhanced exercise performance with Alk. Thus Alk was associated with improved regulation of K+, Na+, Cl- and Lac-.

Alkalosis↗
PubMed2003

Metabolic alkalosis and myoclonus.

This is the first case reported of vomiting-induced metabolic alkalosis associated with myoclonus. The report describes an unusual presentation of myoclonus secondary to acid-base disturbance caused by recreational drug-induced vomiting. The severe derangement of hyponatraemia, hypokalaemia, and alkalosis appears to have been reasonably well tolerated due to the gradual onset and relatively long history. The causes, mechanism, and management of metabolic alkalosis are discussed.

Acid-Base Imbalance↗
PubMed1986

Renal tissue metabolism in the rat during chronic metabolic alkalosis: importance of glycolysis.

Chronic metabolic alkalosis was induced in rats drinking 0.3 M NaHCO3 and receiving 1 mg furosemide/100 g body weight per day intraperitoneally. Another group of animals received a potassium supplement in the form of 0.3 M KHCO3. In this group, hypokalemia did not develop and muscle potassium fell by only 18% versus 50% in those not receiving potassium. In vitro renal production of ammonia and uptake of glutamine fell by 40% with a decrease in the activity of glutaminase I and glutamate dehydrogenase. Activity of phosphofructokinase, a major enzyme of glycolysis, rose only in the kidney of animals receiving a potassium supplement. Fructose-1,6-diphosphatase fell as well as phosphoenolpyruvate carboxykinase. Malate dehydrogenase also fell. The activity of phosphofructokinase also rose in the liver, heart, and leg muscle. The major biochemical changes in the renal cortex were the following: glutamate, alpha-ketoglutarate, malate, lactate, pyruvate, alanine, aspartate, and citrate rose as well as calculated oxaloacetate. The concentration of intermediates like 2-phosphoglycerate, 3-phosphoglycerate, and glucose-6-phosphate fell. The cytosolic redox potential (NAD+/NADH) decreased. In addition to the fall in ammoniagenesis, it could be demonstrated in vitro that the renal tubules incubated with glutamine showed decreased glucose production and increased production of lactate and pyruvate. The concentration of lactate was elevated in all tissues examined including liver, heart, and leg muscle. This study confirms in the rat that decreased renal ammoniagenesis takes place following decreased uptake of glutamine in metabolic alkalosis. All other changes are accounted for by the process of increased glycolysis, which appears to take place in all tissues in metabolic alkalosis.(ABSTRACT TRUNCATED AT 250 WORDS)

Alkalosis↗
PubMed1988

Glucose and lactate turnover and gluconeogenesis in chronic metabolic acidosis and alkalosis in normal and diabetic dogs.

The turnover rate of glucose, the irreversible disposal rate of lactate, and the rate of gluconeogenesis from lactate were calculated by tracer methods in four normal and four alloxan-diabetic dogs under control conditions as well as in chronic, stable metabolic acidosis and alkalosis. Acidosis was produced by feeding dogs 0.8-1 g.kg-1.day-1NH4Cl over 1 week, alkalosis was produced by feeding dogs a chloride-free diet and injections of furosemide. Mean plasma pH in the three states were 7.28 +/- 0.013, 7.40 +/- 0.024, and 7.51 +/- 0.015 in normal dogs, and 7.22 +/- 0.025, 7.42 +/- 0.009, and 7.49 +/- 0.002 in the diabetic dogs. Respective mean plasma bicarbonate levels were 14.6 +/- 0.88, 22.0 +/- 0.80, and 32.4 +/- 1.88 mequiv. in normal dogs, and 12.3 +/- 1.30, 22.6 +/- 0.66, and 35.0 +/- 1.14 mequiv. in diabetic animals. In normal dogs shifts in acid-base balance had no effect on the level of plasma glucose or the turnover rate of glucose. In diabetic dogs plasma glucose level was significantly elevated by alkalosis. Plasma lactate was positively correlated with plasma pH (r = 0.69, p less than 0.01) and was in general higher in diabetic than in normal animals. The increment in concentration was due to a decreased clearance of lactate from the plasma. The irreversible disposal rate was not changed by the acid-base status. Whereas a larger fraction of lactate removed from the plasma appeared in glucose in diabetic animals, this fraction was not changed significantly by shifts in the acid-base status.(ABSTRACT TRUNCATED AT 250 WORDS)

Acidosis↗