Correction of metabolic alkalosis by HCl and acetazolamide: effects on extracellular and intracellular acid-base status in ratsin vivo

1986 ◽  
Vol 30 (7) ◽  
pp. 566-570 ◽  
Author(s):  
K. F. Rothe ◽  
N. Heiler
Keyword(s):  
Metabolic Alkalosis ◽  
Acid Base ◽  
Acid Base Status ◽  
Intracellular Acid

scholarly journals KIDNEY AND URINARY BLADDER RESPONSES OF FRESHWATER RAINBOW TROUT TO ISOSMOTIC NaCl AND NaHCO3 INFUSION

1992 ◽  
Vol 173 (1) ◽  
pp. 181-203 ◽  
Author(s):  
B. James-Curtis ◽  
C. M. Wood
Keyword(s):  
Rainbow Trout ◽  
Urinary Bladder ◽  
Metabolic Alkalosis ◽  
Bladder Function ◽  
Acid Base ◽  
Burst Frequency ◽  
Arterial Ph ◽  
Acid Base Status ◽  
Nacl Load ◽  
Kidney Functions

The relative roles of the kidney and urinary bladder in ion, fluid and acid-base regulation were examined in freshwater rainbow trout chronically infused with either 140 mmol l-1 NaCl or 140 mmol l-1 NaHCO3 (3 ml kg-1 h-1) for 32 h. NaCl had a negligible effect on blood ionic and acid-base status, whereas NaHCO3 induced a metabolic alkalosis characterized by a rise in arterial pH and [HCO3-] and an equimolar fall in [Cl-]. Urine was collected via either an internal catheter, which bypassed bladder function, or an external urinary catheter, which collected naturally voided urine. As a percentage of the infusion rate, glomerular filtration rate increased by about 135 %, but urine flow rate (UFR) by only 80 %, reflecting increased tubular reabsorption of H2O. During NaCl infusion, virtually all of the extra Na+ and Cl- filtered was reabsorbed by the kidney tubules, resulting in an increased UFR with largely unchanged composition. During NaHCO3 infusion, tubular Na+ and Cl- reabsorption again kept pace with filtration. HCO3- reabsorption also increased, but did not keep pace with filtration; an increased flow of HCO3--rich urine resulted, which excreted about 10 % of the infused base load. At rest, fish fitted with external catheters voided in discrete bursts of about 0.85 ml kg-1 at 25 min intervals. During infusion, burst frequency increased by about 40 % and burst volume by about 20 %. Reabsorption by the bladder reduced UFR by 25 %, the excretion of Na+ and Cl- by 50 %, of K+ by 44 % and of urea by 25 %. These differences persisted on a relative basis during NaCl and NaHCO3 infusion despite the decreased residence time. However, HCO3- was neither secreted nor reabsorbed by the bladder. We conclude that the freshwater kidney functions to remove as much NaCl as possible from the urine, regardless of the NaCl load, and this role is supplemented by bladder function. The bladder plays no role in acid-base regulation during metabolic alkalosis.

White Muscle Intracellular Acid-Base and Lactate Status Following Exhaustive Exercise: A Comparison between Freshwater- and Sea Water- Adapted Rainbow Trout

1991 ◽  
Vol 156 (1) ◽  
pp. 153-171 ◽  
Author(s):  
YONG TANG ◽  
ROBERT G. BOUTILIER
Keyword(s):  
Rainbow Trout ◽  
White Muscle ◽  
Sea Water ◽  
Ph Regulation ◽  
Recovery Period ◽  
Exhaustive Exercise ◽  
Acid Base ◽  
Post Exercise ◽  
Acid Base Status ◽  
Intracellular Acid

The intracellular acid-base status of white muscle of freshwater (FW) and seawater (SW) -adapted rainbow trout was examined before and after exhaustive exercise. Exhaustive exercise resulted in a pronounced intracellular acidosis with a greater pH drop in SW (0.82 pH units) than in FW (0.66 pH units) trout; this was accompanied by a marked rise in intracellular lactate levels, with more pronounced increases occurring in SW (54.4 mmoll−1) than in FW (45.7 mmoll−1) trout. Despite the more severe acidosis, recovery was faster in the SW animals, as indicated by a more rapid clearance of metabolic H+ and lactate loads. Compartmental analysis of the distribution of metabolic H+ and lactate loads showed that the more rapid recovery of pH in SW trout could be due to (1) their greater facility for excreting H+ equivalents to the environmental water [e.g. 15.5 % (SW) vs 5.0 % (FW) of the initial H+ load was stored in external water at 250 min post-exercise] and, to a greater extent, (2) the more rapid removal of H+, facilitated via lactate metabolism in situ (white muscle) and/or the Cori cycle (e.g. heart, liver). The slower pH recovery in FW trout may also be due in part to greater production of an ‘unmeasured acid’ [maximum approx. 8.5 mmol kg−1 fish (FW) vs approx. 6 mmol kg−1 fish (SW) at 70–130 min post-exercise] during the recovery period. Furthermore, the analysis revealed that H+-consuming metabolism is quantitatively the most important mechanism for the correction of an endogenously originating acidosis, and that extracellular pH normalization gains priority over intracellular pH regulation during recovery of acid-base status following exhaustive exercise.

scholarly journals Acid base status of prevalent peritoneal dialysis patients

2018 ◽  
Vol 1 (1) ◽  
pp. 21-25
Author(s):  
Raymond Azar ◽  
Vincent Coevoet
Keyword(s):  
Peritoneal Dialysis ◽  
Metabolic Acidosis ◽  
Metabolic Alkalosis ◽  
Lower Probability ◽  
Individual Choice ◽  
Dietary Intakes ◽  
Dialysis Patients ◽  
Acid Base Balance ◽  
Acid Base ◽  
Acid Base Status

Acid-base status of patients on peritoneal dialysis is influenced by multiple factors. Metabolic acidosis is a common feature of chronic renal failure and dialysis treatment provides alkali in the dialysate in order to maintain a normal acid-base balance. This paper reports the prevalence of acid-base disorders in peritoneal dialysis patients and their associations with clinical and laboratory parameters. This is a cross-sectional retrospective study that included all PD patients registered in the RDPLF database. Metabolic acidosis was found in 20.4% of patients while 27.8% of patients had metabolic alkalosis. There is a significant relationship between age, protein intake estimated by nPNA and the level of alkaline reserve pleading in favor of the influence of dietary intakes in the maintenance of metabolic acidosis. Low residual renal function is associated with a lower probability of being in metabolic alkalosis. These results could allow an individual choice of the dialysate buffer in order to permanently obtain stable acid-base status in patients on peritoneal dialysis.

scholarly journals Life-threatening metabolic alkalosis in Pendred syndrome

2011 ◽  
Vol 165 (1) ◽  
pp. 167-170 ◽  
Author(s):  
Narayanan Kandasamy ◽  
Laura Fugazzola ◽  
Mark Evans ◽  
Krishna Chatterjee ◽  
Fiona Karet
Keyword(s):  
Metabolic Alkalosis ◽  
Collecting Duct ◽  
Sensorineural Deafness ◽  
Apical Plasma Membrane ◽  
Cortical Collecting Duct ◽  
Loss Of Function ◽  
Pendred Syndrome ◽  
Acid Base ◽  
Life Threatening ◽  
Acid Base Status

IntroductionPendred syndrome, a combination of sensorineural deafness, impaired organification of iodide in the thyroid and goitre, results from biallelic defects in pendrin (encoded by SLC26A4), which transports chloride and iodide in the inner ear and thyroid respectively. Recently, pendrin has also been identified in the kidneys, where it is found in the apical plasma membrane of non-α-type intercalated cells of the cortical collecting duct. Here, it functions as a chloride–bicarbonate exchanger, capable of secreting bicarbonate into the urine. Despite this function, patients with Pendred syndrome have not been reported to develop any significant acid–base disturbances, except a single previous reported case of metabolic alkalosis in the context of Pendred syndrome in a child started on a diuretic.Case reportWe describe a 46-year-old female with sensorineural deafness and hypothyroidism, who presented with severe hypokalaemic metabolic alkalosis during inter-current illnesses on two occasions, and who was found to be homozygous for a loss-of-function mutation (V138F) in SLC26A4. Her acid–base status and electrolytes were unremarkable when she was well.ConclusionThis case illustrates that, although pendrin is not usually required to maintain acid–base homeostasis under ambient condition, loss of renal bicarbonate excretion by pendrin during a metabolic alkalotic challenge may contribute to life-threatening acid–base disturbances in patients with Pendred syndrome.

Blood Gases, and Extracellular/Intracellular Acid-Base Status as a Function of Temperature in the Anuran Amphibians Xenopus Laevis and Bufo Marinus

1987 ◽  
Vol 130 (1) ◽  
pp. 13-25 ◽  
Author(s):  
R. G. BOUTILIER ◽  
M. L. GLASS ◽  
N. HEISLER
Keyword(s):  
Xenopus Laevis ◽  
Blood Gases ◽  
Bufo Marinus ◽  
Temperature Dependent ◽  
Acid Base ◽  
Anuran Amphibians ◽  
Acid Base Status ◽  
Arterial Plasma ◽  
Tissue Compartments ◽  
Intracellular Acid

Blood gases, and parameters of the extracellular and intracellular acid-base status, were measured in the anuran amphibians Bufo marinus and Xenopus laevis acclimated to temperatures of 10, 20 and 30°C for 12 days. Arterial POO2 rose with temperature so that approximately constant oxygen saturation of the blood was maintained, a phenomenon explained on the basis of models for O2 transport in animals with central vascular shunts and temperature-dependent shifts in O2 equilibrium characteristics. Arterial plasma pH of both species varied inversely with temperature, the pH/temperature coefficient being not significantly different from that required for constant relative alkalinity or dissociation of imidazole. The change in plasma pH was brought about mainly by changes in PCOCO2 although plasma bicarbonate concentration also changed significantly. Intracellular pH/temperature relationships were found to be non-linear in most of the tissues. There was considerable variability among body tissue compartments and between the two species. These data confirm that the various tissue compartments in ectotherms maintain unique ΔpH/Δt relationships, and indicate that measurement of extracellular pH as a function of temperature is not a good indicator for alphastat-type, temperature-dependent, acid-base regulation.

scholarly journals Acid-Base Status Disturbances in Patients on Chronic Hemodialysis at High Altitudes

2018 ◽  
Vol 2018 ◽  
pp. 1-5 ◽  
Author(s):  
Javier Enrique Cely ◽  
Oscar G. Rocha ◽  
María J. Vargas ◽  
Rafael M. Sanabria ◽  
Leyder Corzo ◽  
...  
Keyword(s):  
Metabolic Acidosis ◽  
Metabolic Alkalosis ◽  
Base Excess ◽  
Chronic Hemodialysis ◽  
High Altitudes ◽  
Acid Base ◽  
Arterial Blood ◽  
Base Disorder ◽  
Acid Base Status ◽  
Normal Acid

Background. Acid-base disorders have been previously described in patients with chronic hemodialysis, with metabolic acidosis being the most important of them; however, little is known about the potential changes in acid-base status of patients on dialysis living at high altitudes. Methods. Cross-sectional study including 93 patients receiving chronic hemodialysis on alternate days and living in Bogotá, Colombia, at an elevation of 2,640 meters (8,661 feet) over sea level (m.o.s.l.). Measurements of pH, PaCO2, HCO3, PO2, and base excess were made on blood samples taken from the arteriovenous fistula (AVF) during the pre- and postdialysis periods in the midweek hemodialysis session. Normal values for the altitude of Bogotá were taken into consideration for the interpretation of the arterial blood gases. Results. 43% (n= 40) of patients showed predialysis normal acid-base status. The most common acid-base disorder in predialysis period was metabolic alkalosis with chronic hydrogen ion deficiency in 19,3% (n=18). Only 9,7% (n=9) had predialysis metabolic acidosis. When comparing pre- and postdialysis blood gas analysis, higher postdialysis levels of pH (7,41 versus 7,50, p<0,01), bicarbonate (21,7mmol/L versus 25,4mmol/L, p<0,01), and base excess (-2,8 versus 2,4, p<0,01) were reported, with lower levels of partial pressure of carbon dioxide (34,9 mmHg versus 32,5 mmHg, p<0,01). Conclusion. At an elevation of 2,640 m.o.s.l., a large percentage of patients are in normal acid-base status prior to the dialysis session (“predialysis period”). Metabolic alkalosis is more common than metabolic acidosis in the predialysis period when compared to previous studies. Paradoxically, despite postdialysis metabolic alkalosis, PaCO2 levels are lower than those found in the predialysis period.

Respiratory effects in humans of a 5-day elevation of end-tidal PCO2 by 8 Torr

2003 ◽  
Vol 95 (5) ◽  
pp. 1947-1954 ◽  
Author(s):  
Alexi Crosby ◽  
Nick P. Talbot ◽  
George M. Balanos ◽  
Simon Donoghue ◽  
Marzieh Fatemian ◽  
...  
Keyword(s):  
Metabolic Alkalosis ◽  
Feedback Loop ◽  
Human Subjects ◽  
Acute Hypoxia ◽  
Acid Base ◽  
Healthy Human ◽  
Respiratory Effects ◽  
Healthy Human Subjects ◽  
Acid Base Status ◽  
End Tidal

The aims of this study were to determine 1) whether ventilatory adaptation occurred over a 5-day exposure to a constant elevation in end-tidal Pco2 and 2) whether such an exposure altered the sensitivity of the chemoreflexes to acute hypoxia and hypercapnia. Ten healthy human subjects were studied over a period of 13 days. Their ventilation, chemoreflex sensitivities, and acid-base status were measured daily before, during, and after 5 days of elevated end-tidal Pco2 at 8 Torr above normal. There was no major adaptation of ventilation during the 5 days of hypercapnic exposure. There was an increase in ventilatory chemosensitivity to acute hypoxia (from 1.35 ± 0.08 to 1.70 ± 0.07 l/min/%; P < 0.01) but no change in ventilatory chemosensitivity to acute hypercapnia. There was a degree of compensatory metabolic alkalosis. The results do not support the hypothesis that the ventilatory adaptation to chronic hypercapnia would be much greater with constant elevation of alveolar Pco2 than with constant elevation of inspired Pco2, as has been used in previous studies and in which the feedback loop between ventilation and alveolar Pco2 is left intact.

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