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PubMed1977

Effects of saline infusion and acute metabolic acidosis and alkalosis on water and electrolyte transport in the human colon.

Both the kidney and colon secrete bicarbonate and transport water and electrolytes. The respective contributions of these two organs to acid-base and electrolyte balance in normal man has thus been studied in eight healthy male volunteers who underwent simultaneous renal clearance studies, and colonic perfusion with a 0.9% saline or 7.2% mannitol solution, during metabolic alkalosis and acidosis, extracellular volume expansion, and control conditions. There was no influence of these acid-base conditions on electrolyte transport in the colon. In the urine, preferential loss of chloride over sodium averaged 81, 143 (P less than 0.001), and 141 (P less than 0.05) muequiv./min, during control, metabolic acidosis, and extracellular volume expansion conditions, respectively. During alkalosis more sodium than chloride was lost (146 muequiv./min) (P less than 0.001). Colonic pH averaged 7.41 during saline and 6.75 (P less than 0.005) during mannitol perfusion. Titratable acid was not produced in the colon during saline perfusion, and averaged 18 muequiv./min during mannitol perfusion. Urinary titratable acid increased from 19 to 25 muequiv./min (P less than 0.01) during volume expansion. With saline perfusion, bicarbonate secretion rate in the colon rose from 249 muequiv./min during control conditions to 289 muequiv./min during metabolic alkalosis (P less than 0.05). More bicarbonate was excreted in the urine during alkalosis when mannitol was introduced in the colon (243 muequiv./min) than when saline was perfused (152 muequiv./min) (P less than 0.05). This study indicates that the response of the human colon is trivial compared with that of the kidney during acute changes in acid-base balance.

Acid-Base Equilibrium↗
PubMed1989

Effects of chronic metabolic alkalosis on Ca2+, PTH and 1,25(OH)2D3 in the rat.

The effect of chronic metabolic alkalosis on arterial blood ionized calcium concentration ([Ca2+]) and the levels of serum parathyroid hormone (PTH) and 1,25-dihydroxyvitamin D3 [1,25(OH)2D3] is difficult to predict. Although a fall in pH directly decreases [Ca2+], chronic alkalosis reduces urine calcium excretion, which could elevate [Ca2+]. [Ca2+] modulates the serum level of PTH and the level of 1,25(OH)2D3 directly and through PTH. To determine the effect of chronic metabolic alkalosis on [Ca2+], PTH, and 1,25(OH)2D3, rats were made alkalemic by feeding a chloride-deficient diet (LCl) or LCl with 75 mM NaHCO3 in the drinking water (LCl + HCO3-) and compared with controls fed a chloride-replete diet (NCl). Compared with NCl, after 8 days of LCl and LCl + HCO3- arterial pH and PTH rose and [Ca2+] fell. Serum 1,25(OH)2D3 tended to rise with LCl and rose with LCl + HCO3-. Serum 1,25(OH)2D3 was correlated inversely with [Ca2+] (r = -0.510, n = 54, P less than 0.001) and with pH (r = -0.291, n = 57, P less than 0.03) but not with PTH or phosphorus. Stepwise regression analysis indicated that [Ca2+] accounted for the majority of the variance of serum 1,25(OH)2D3. Chronic metabolic alkalosis induced by a low-chloride diet and HCO3- appears to increase serum PTH and 1,25(OH)2D3 through a fall in [Ca2+].

Alkalosis↗
PubMed1982

Effect of acute respiratory alkalosis and acidosis on intestinal ion transport in vivo.

The effects of acute respiratory alkalosis and acidosis on intestinal electrolyte transport were studied in adult Sprague-Dawley rats. During in situ intestinal perfusion, anesthetized animals were ventilated with 0, 3, or 8% CO2, creating states of alkalosis (pH 7.64 +/- 0.01), normocapnia (pH 7.45 +/- 0.01), or acidosis (pH 7.26 +/- 0.01), respectively. The plasma bicarbonate concentration decreased 2.0 mM during alkalosis and increased 2.1 mM during acidosis. The jejunum did not respond to the acid-base disturbances. In both the ileum and colon, alkalosis decreased the net absorption of water (-16%), sodium (-23%), and chloride (-42%) and the net secretion of bicarbonate (-33%), whereas acidosis had the opposite effect, i.e., the net absorption of water (41%), sodium (39%), and chloride (32%) increased as did net bicarbonate secretion (33%) (ileal values given). Changes in sodium chloride movement could be correlated with changes in systemic pH and CO2 tension (PCO2), and bicarbonate secretion paralleled changes in the plasma bicarbonate concentration. The acid-base disorders had no effect on ileal and colonic net potassium secretion and transmural potential difference. These studies suggest that systemic pH and/or PCO2 regulate sodium chloride absorption, and the plasma bicarbonate concentration regulates bicarbonate secretion.

Acidosis, Respiratory↗
PubMed2002

Alkalosis stimulates endothelial nitric oxide synthase in cultured human pulmonary arterial endothelial cells.

To investigate the effect of extracellular pH on endothelial nitric oxide synthase (eNOS) in human pulmonary arteries, we measured eNOS activity and expression as well as some ion channels in human pulmonary arterial endothelial cells (HPAEC) exposed to various pH levels (6.6-8.0). eNOS activity was found to increase with alkalization and decrease with acidification, while Ca2+ uptake into HPAEC increased with alkalization. The addition of 3',4'-dichlorobenzamil hydrochloride, an inhibitor of the Na+/Ca2+ exchanger (NCX), prevented the increase of eNOS activity with alkalosis. Exposure to alkalosis and acidosis increased eNOS and NCX mRNA levels. These results suggest that an elevation of extracellular pH activates eNOS via the influx of extracellular Ca2+ and that NCX also regulates eNOS activity during alkalosis. Furthermore, NCX may have a tight interaction with eNOS at the level of transcription and might affect pulmonary circulation during alkalosis and acidosis.

Acidosis↗
PubMed1980

HCO3-Cl exchange transport in the adaptive response to alkalosis by turtle bladder.

The isolated turtle urinary bladder acidifies its mucosal (M) solution, and the rate of acidification (JH) is equivalent to the short-circuit current after Na+ transport is abolished by ouabain. When HCO3(-) is present in the serosal solution it is secreted into M in an electroneutral exchange for absorbed Cl-. The rate of HCO3(-) secretion (JHCO3(-)) can be measured by pH stat titration after JH is nullified by an opposing pH gradient. With use of these methods JH and JHCO3 were measured sequentially in bladdes from control animals and animals fed NaHCO3 (alkalosis) or NH4Cl (acidosis). JH in alkalosis (57 +/- 6 micro A) was ot different from control values (53 +/- 7 micro A). JHCO3, however, was nearly 40% higher in alkalosis (1.63 +/- 0.11 vs. 1.17 +/- 0.14 mu mol x h-1 x 8 cm-2). In contrast, JHCO3 in acidosis was similar to control values (0.89 +/- 0.15 mu mol x h-1 x 8 cm-2) but JH was increased. As judged from Cl- fluxes, neither alkalosis nor acidosis altered the electroneutral coupling between HCO3(-) secretion and Cl- absorption. JH and JHCO3 appear to be independent processes in the turtle bladder that are capable of responding independently to physiologic changes in the acid-base status of the intact animal.

Absorption↗
PubMed1980

Relationship of CSF pH, O2, and CO2 responses in metabolic acidosis and alkalosis in humans.

The effect of induced metabolic acidosis (48 h of NH4Cl ingestion, BE - 10.6 +/- 1.1) and alkalosis (43 h of NaHCO3- ingestion BE 8.8 +/- 1.6) on arterial and lumber CSF pH, Pco2, and HCO3- and ventilatory responses to CO2 and to hypoxia was assessed in five healthy men. In acidosis lumbar CSF pH rose 0.033 +/- 0.02 (P less than 0.05). In alkalosis CSF pH was unchanged. Ventilatory response lines to CO2 at high O2 were displaced to the left in acidosis (9.0 +/- 1.4 Torr) and to the right in alkalosis (4.5 +/- 1.5 Torr) with no change in slope. The ventilatory response to hypoxia (delta V40) was increased in acidosis (P less than 0.05) and it was decreased in four subjects in alkalosis (P, not significant). We conclude that the altered ventilatory drives of steady-state metabolic imbalance are mediated by peripheral chemoreceptors, and in acidosis the medullary respiratory chemoreceptor drive is decreased.

Acidosis↗
PubMed1990

Compensation of respiratory alkalosis induced after acclimation to simulated altitude.

Conscious intact rats previously acclimated for 3 wk to barometric pressure of 370-380 Torr (3WHx) were made alkalotic for 3 h by a decrease in inspired O2 fraction from 0.10 to 0.075 at ambient barometric pressure (730-740 Torr). Controls were normoxic littermates (Nx) in which inspired O2 fraction was lowered from approximately 0.21 to 0.10 for 3 h. Arterial PCO2 decreased progressively and similarly in both groups (65-70% of control at 15 min). Initially, arterial pH increased less in 3WHx (0.09 +/- 0.004 vs. 0.15 +/- 0.008). As hypocapnia continued, delta[HCO3-]/delta pH (mmol.l-1.pH) became more negative in Nx, from -15.2 +/- 2.5 at 15 min to -37.0 +/- 2.9 at 3 h, indicating nonrespiratory compensation of alkalosis. In 3WHx, delta[HCO3-]/delta pH did not change during alkalosis. Cumulative renal excretion of base (mueq/100 g) during alkalosis increased by 73.2 +/- 11.1 in Nx and 25.4 +/- 7.3 in 3WHx. This difference was mainly due to a larger increase in HCO3- excretion in Nx. The data suggest that the smaller compensation of hypocapnic alkalosis in 3WHx is partly due to the smaller increase in renal base excretion. Because base availability limits renal base excretion, the smaller renal response of 3WHx may be secondary to the low plasma HCO3- concentration that accompanies altitude acclimation.

Acid-Base Equilibrium↗
PubMed2004

Hypokalemia and alkalosis in adipsic hypernatremia are not associated with hyperaldosteronism.

Idiopathic adipsic hypernatremia (AH) is a rare disorder associated with hypokalemia and alkalosis. Hypokalemic alkalosis has been presumed to be secondary to hyperaldosteronism. We evaluated plasma renin activity, serum aldosterone, serum and urine electrolytes in a 17-year-old patient with AH on several occasions. Despite evidence of mild dehydration, serum Na >160 and K <3.2, aldosterone levels were suppressed and plasma renin activity was not elevated. Urine Na and K were not conserved. We also examined electrolyte and hormone levels in previously reported cases of AH. Aldosterone levels were not increased in any of the cases when measured. Renin secretion was increased in 2 patients. Among the compiled cases serum K was inversely correlated with serum Na (r = -0.73, p < 0.002, n = 15). Hypokalemia and alkalosis occurring in AH are not associated with secondary hyperaldosteronism. Patients with AH may have chronic renal losses of potassium leading to hypokalemia and alkalosis.

Adolescent↗
PubMed2000

Injurious effects of hypocapnic alkalosis in the isolated lung.

Mechanical ventilation can worsen morbidity and mortality by causing ventilator-associated lung injury, especially where adverse ventilatory strategies are employed. Adverse strategies commonly involve hyperventilation, which frequently results in hypocapnia. Although hypocapnia is associated with significant lung alterations (e.g., bronchospasm, airway edema), the effects on alveolar-capillary permeability are unknown. We investigated whether hypocapnia could cause lung injury independent of altering ventilatory strategy. We hypothesized that hypocapnia would cause lung injury during prolonged ventilation, and would worsen injury following ischemia-reperfusion. We utilized the isolated buffer-perfused rabbit lung model. Pilot studies assessed a range of levels of hypocapnic alkalosis. Experimental preparations were randomized to control groups (FI(CO(2)) = 0.06) or groups with hypocapnia (FI(CO(2)) = 0.01). Following prolonged ventilation, pulmonary artery pressure, airway pressure, and lung weight were unchanged in the control group but were elevated in the group with hypocapnia; elevation in microvascular permeability was greater in the hypocapnia versus control groups. Injury following ischemia-reperfusion was significantly worse in the hypocapnia versus control groups. In a preliminary series, degree of lung injury was proportional to the degree of hypocapnic alkalosis. We conclude that in the current model (1) hypocapnic alkalosis is directly injurious to the lung and (2) hypocapnic alkalosis potentiates ischemia-reperfusion-induced acute lung injury.

Alkalosis↗
PubMed1985

Does intermittent mandatory ventilation correct respiratory alkalosis in patients receiving assisted mechanical ventilation?

One of the claimed advantages of intermittent mandatory ventilation (IMV) over assisted mechanical ventilation (AMV) (assist-control) is the avoidance or correction of acute respiratory alkalosis, ostensibly by allowing patients to achieve normal alveolar ventilation (VA) and PaCO2 through the function of an intact ventilatory drive. However, although respiratory alkalosis in patients being hyperventilated with controlled mechanical ventilation (CMV) can be corrected by a change to IMV, CMV is seldom appropriate for patients with acute respiratory failure, and whether IMV affects respiratory alkalosis in patients triggering the ventilator in the AMV mode has not previously been tested. We studied 26 patients with acute respiratory alkalosis (pH greater than or equal to 7.48) while receiving AMV. Measurements of arterial blood gases and CO2 production (VCO2), and calculation of VA, were performed after 30 min of AMV, repeated after 30 min of IMV at a mandatory rate one half the previous AMV rate, and then repeated again 30 min after a return to the original AMV settings. Mean arterial pH decreased slightly from 7.51 during AMV to 7.48 during IMV, and returned to 7.51 on resumption of AMV (p less than 0.05 for both changes); corresponding mean values for PaCO2 were 28.6, 29.7, and 27.5 mmHg, respectively. These changes were related to an increase in VCO2 during IMV as compared with AMV (p less than 0.05), without a significant alteration in VA. When the mandatory rate was further reduced during IMV from one half to one fourth the prior, triggered AMV rate in 10 patients, no additional reduction in pH occurred.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1973

Glucose utilization and production by the dog kidney in vivo in metabolic acidosis and alkalosis.

Using D-[1-(14)C]glucose as a tracer, renal glucose utilization and production was measured in chronic metabolic acidosis and alkalosis in dog kidney in vivo. In six experiments in acidosis, mean total renal glucose production was 4.447+/-1.655 SE mumol/min and glucose utilization was 4.187+/-0.576 SE mumol/min. In five alkalotic experiments it was found that mean total glucose production was 12.227+/-2.026 SE mumol/min and glucose utilization was 18.186+/-2.054 SE mumol/min. Renal glucose utilization and production are therefore significantly higher in alkalosis than in acidosis in vivo. Since glucose production is maximal under conditions when glutamine extraction is minimal (i.e. alkalosis), it is apparent that in alkalosis glutamine is not a major precursor of glucose.

Acidosis↗
PubMed2006

Acetazolamide-mediated decrease in strong ion difference accounts for the correction of metabolic alkalosis in critically ill patients.

INTRODUCTION: Metabolic alkalosis is a commonly encountered acid-base derangement in the intensive care unit. Treatment with the carbonic anhydrase inhibitor acetazolamide is indicated in selected cases. According to the quantitative approach described by Stewart, correction of serum pH due to carbonic anhydrase inhibition in the proximal tubule cannot be explained by excretion of bicarbonate. Using the Stewart approach, we studied the mechanism of action of acetazolamide in critically ill patients with a metabolic alkalosis. METHODS: Fifteen consecutive intensive care unit patients with metabolic alkalosis (pH > or = 7.48 and HCO3- > or = 28 mmol/l) were treated with a single administration of 500 mg acetazolamide intravenously. Serum levels of strong ions, creatinine, lactate, weak acids, pH and partial carbon dioxide tension were measured at 0, 12, 24, 48 and 72 hours. The main strong ions in urine and pH were measured at 0, 3, 6, 12, 24, 48 and 72 hours. Strong ion difference (SID), strong ion gap, sodium-chloride effect, and the urinary SID were calculated. Data (mean +/- standard error were analyzed by comparing baseline variables and time dependent changes by one way analysis of variance for repeated measures. RESULTS: After a single administration of acetazolamide, correction of serum pH (from 7.49 +/- 0.01 to 7.46 +/- 0.01; P = 0.001) was maximal at 24 hours and sustained during the period of observation. The parallel decrease in partial carbon dioxide tension was not significant (from 5.7 +/- 0.2 to 5.3 +/- 0.2 kPa; P = 0.08) and there was no significant change in total concentration of weak acids. Serum SID decreased significantly (from 41.5 +/- 1.3 to 38.0 +/- 1.0 mEq/l; P = 0.03) due to an increase in serum chloride (from 105 +/- 1.2 to 110 +/- 1.2 mmol/l; P < 0.0001). The decrease in serum SID was explained by a significant increase in the urinary excretion of sodium without chloride during the first 24 hours (increase in urinary SID: from 48.4 +/- 15.1 to 85.3 +/- 7.7; P = 0.02). CONCLUSION: A single dose of acetazolamide effectively corrects metabolic alkalosis in critically ill patients by decreasing the serum SID. This effect is completely explained by the increased renal excretion ratio of sodium to chloride, resulting in an increase in serum chloride.

Acetazolamide↗
PubMed1979

A short communication. Congenital renal alkalosis.

Patients with idiopathic hypokalemic metabolic alkalosis and hyperrenienmia have been lumped under the heading of Bartter's syndrome. However, the clinical picture is not totally uniform. Recently, Gullner et al. described a familial disorder with hypokalemic metabolic alkalosis, hyperreninemia, and aldosteronism, but without juxtaglomerular hyperplasia. They suggested that this family had a condition other than Bartter's syndrome. The present report details the followup from infancy to adulthood of a patient with hypokalemic metabolic alkalosis, salt wasting, and hyperreninemia, but with normal aldosterone level and without juxtaglomerular hyperplasia. The authors suggest that this new condition be termed renal alkalosis. The studies suggest that the distal tubular reabsorptive capacity was defective in this patient.

Adolescent↗
PubMed2003

Metabolic alkalosis contributes to acute hypercapnic respiratory failure in adult cystic fibrosis.

BACKGROUND: and study objectives: Patients with end-stage cystic fibrosis (CF) develop respiratory failure and hypercapnia. In contrast to COPD patients, altered electrolyte transport and malnutrition in CF patients may predispose them to metabolic alkalosis and, therefore, may contribute to hypercapnia. The aim of this study was to determine the prevalence of metabolic alkalosis in adults with hypercapnic respiratory failure in the setting of acute exacerbations of CF compared with COPD. DESIGN: Levels of arterial blood gases, plasma electrolytes, and serum albumin from 14 consecutive hypercapnic CF patients who had been admitted to the hospital with a respiratory exacerbation were compared with 49 consecutive hypercapnic patients with exacerbations of COPD. Hypercapnia was defined as a PaCO(2) of > or = 45 mm Hg. RESULTS: Despite similar PaCO(2) values, patients in the CF group were significantly more alkalotic than were those in the COPD group (mean [+/- SD] pH, 7.43 +/- 0.03 vs 7.37 +/- 0.05, respectively; p < 0.01). A mixed respiratory acidosis and metabolic alkalosis was evident in 71% of CF patients and 22% of COPD patients (p < 0.01). The mean concentrations of plasma chloride (95.1 +/- 4.9 vs 99.8 +/- 5.2 mmol/L, respectively; p < 0.01) and sodium (136.5 +/- 2.8 vs 140.4 +/- 4.5 mmol/L, respectively; p < 0.01) were significantly lower in the CF group, and the levels of serum albumin were significantly reduced (27.4 +/- 5.8 vs 33.7 +/- 4.8 mmol/L, respectively; p < 0.01). CONCLUSION: Metabolic alkalosis contributes to hypercapnic respiratory failure in adults with acute exacerbations of CF. This acid-base disturbance occurs in conjunction with reduced total body salt levels and hypoalbuminemia.

Acidosis, Respiratory↗
PubMed1986

Two cases of saline-responsive metabolic alkalosis associated with high urinary chloride concentrations.

Two particular cases of saline-responsive metabolic alkalosis associated with high urinary chloride concentrations were documented. In the first case, pseudoaldosteronism with long term glycylrrhetinic acid ingestion, and in the second case, probably salt losing nephropathy with extracellular fluid volume contraction were the putative causes of metabolic alkalosis, respectively. Sodium chloride loading with saline (0.9% NaCl) infusion to these patients corrected the accompanying hypopotassemic metabolic alkalosis. Recent trends in the pathophysiology of both saline-responsive and saline-resistant metabolic alkalosis were discussed.

Aged↗
PubMed1989

Effects of acute metabolic acidosis and alkalosis on leucine metabolism in conscious dogs.

To determine the effects of acute metabolic acidosis and alkalosis on leucine metabolism in vivo, mongrel dogs were infused with [1-14C]leucine for 8 h, along with NaCl, HCI, or NaHCO3 over the last 4 h. Arterial pH did not change from the basal value during NaCl infusion but decreased (P less than .01) and increased (P less than .01) during HCl and NaHCO3 infusions, respectively. Total leucine carbon entry did not change from the basal value during saline infusion but increased (P less than .01) with acidosis and decreased (P less than .05) with alkalosis. Compared with saline controls, acidosis increased (P less than .01) leucine oxidation. During alkalosis decreased (P less than .01) leucine oxidation. During acidosis, total plasma essential and nonessential amino acid concentrations increased (P less than .05), whereas during alkalosis, total plasma essential and nonessential amino acid concentrations decreased (P less than .05). These studies suggest that acute alterations in arterial pH may affect the regulation of protein metabolism in vivo and must be considered in the interpretation of results from experiments in which alterations of acid-base homeostasis may have occurred.

3-Hydroxybutyric Acid↗
PubMed1991

Adaptation to metabolic alkalosis by the turtle urinary bladder.

We studied the mechanism of adaptation to metabolic alkalosis by the turtle urinary bladder in vitro. Turtles were made alkalotic by administration of oral NaHCO3. Bladders removed from alkalotic turtles had an increased rate of HCO3- secretion in vitro as compared with that of control. H+ secretion, however, was not different, indicating that metabolic alkalosis selectively increases HCO3- secretion. Fluorescence microscopy was used to quantify the carbonic anhydrase cells. The total number of carbonic anhydrase cells was determined by mucosal staining of the bladder with 6-carboxyfluorescein diacetate. The number of HCO3(-)-secreting cells (beta cells) was quantified by mucosal staining with NBD-taurine and the number of H(+)-secreting cells (alpha cells) was calculated from the difference between the two. Metabolic alkalosis significantly increased the total number of 6-carboxyfluorescein positive cells and NBD-taurine-positive cells. The increase in the number of 6-carboxyfluorescein positive cells was totally accounted for by the increase in the NBD-taurine-positive cells without change in the number of alpha cells. If NBD-taurine accurately reflects the number of beta cells, these studies show that the adaptation to metabolic alkalosis is mediated, at least in part, by an increase in the number of HCO3(-)-secreting (beta) cells.

Adaptation, Physiological↗
PubMedDate not supplied

Acid-base balance and blood gases changes and "lactate excess" in acute respiratory alkalosis during general anaesthesia.

In 40 young males aged 18-20 years operated on for inguinal hernioplasty acute respiratory alkalosis was obtained in the 45th minute of general anaesthesia. The values of basic acid-base balance parameters, blood gases, pyruvate and lactate levels and "lactate excess" were determined before and after hyperventilation. Shifts in the concentrations of hydrogen and bicarbonate ions were found which are both typical of acute respiratory alkalosis. No changes were observed in the oxygenation of capillary blood and the values of "lactate excess" were normal which rules out tissue hypoxia during acute respiratory alkalosis. Passive hyperventilation being a less dangerous alternative of hypoventilation is a frequent occurrence during general anaesthesia and it causes transient respiratory alkalosis.

Acid-Base Equilibrium↗