Amiloride prevents the metabolic acidosis of a KCl load in nephrectomized rats

1989 ◽  
Vol 76 (6) ◽  
pp. 649-652 ◽  
Author(s):  
Guillermo A. Altenberg ◽  
Patricia C. Aristimuño ◽  
Carlos E. Amorena ◽  
Alberto C. Taquini
Keyword(s):  
Metabolic Acidosis ◽  
Cell Membranes ◽  
Coupling Ratio ◽  
Blood Ph ◽  
Inulin Space

1. Counter movements of K+ and H+ across cell membranes were studied in nephrectomized KCl-loaded rats. In one group of animals, the movements of K+ and H+ were determined during and after a KCl load, and in another group, amiloride was used in order to evaluate Na+ participation in K+/H+ exchange. 2. After a KCl load at constant Pco2, 79% of infused K+ left the inulin space, half of which was in exchange for H+. As a result, blood pH fell from 7.40 ± 0.01 to 7.30 ± 0.01 (mean ± sem; P < 0.001). 3. During KCl infusion, the K+/H+ exchange ratio varied between 1.3 and 6.8, showing that the coupling ratio is not fixed. 4. Amiloride did not change blood pH and plasma [K+], but prevented the metabolic acidosis produced by the KCl load without affecting K+ entry into the non-inulin space. Therefore, K+ and H+ movements became completely dissociated. 5. The results indicate that KCl activates an amiloride-sensitive H+ extrusion from the cells. This finding is compatible with the view that Na+/H+ exchange participates in the metabolic acidosis produced by a KCl load.

scholarly journals Effects of Pyruvate Supplementation on High-intensity Interval Exercise Induced Metabolic Acidosis and Repeated Sprint Exercise Performance of College Soccer Athletes

2021 ◽  
Author(s):  
yanping yang ◽  
Junqiang Qiu ◽  
Mengyue Wang ◽  
Lin Feng ◽  
Dan Luo ◽  
...  
Keyword(s):  
Metabolic Acidosis ◽  
High Intensity ◽  
Energy Contribution ◽  
Sprint Exercise ◽  
Interval Exercise ◽  
Repeated Sprint ◽  
Blood Ph ◽  
High Intensity Interval ◽  
The Impact ◽  
Oxidative System

Abstract Background: The effects of pyruvate on metabolic acidosis and oxidative metabolism had been studied. The ability to attenuate acidosis and improve oxidative system contribution are critical to the performance of team sport athletes during perform multiple high-intensity exercise over a limited period of time. This study aimed to investigate the impact of pyruvate supplementation on energy metabolism and metabolic acidosis during high-intensity interval exercise (HIIE), as well as to evaluate its role on repeated sprint exercise (RSE) performance.Methods: 14 well-trained male college soccer athletes (age: 20 ± 2 years, body fat: 13.11 ± 3.50 %) were studied in a randomized, double-blind, cross-over study. The participants ingested either 0.1g/kg/d of pyruvate or a placebo for 1-week. Metabolic acidosis was induced by HIIE after the supplement period, and RSE ability in the acidosis state was assessed. Venous blood pH, bicarbonate (HCO3-) and base excess (BE) were measured at baseline, pre-HIIE, post-HIIE, pre-RSE and post-RSE. Finger-stick blood lactate were collected at baseline, immediately after each bout of HIIE and 3, 5, 7, 10 min after HIIE. The energy systems contribution during HIIE were estimated. Results: Blood pH, HCO3- and BE were significantly lower than baseline after HIIE (p < 0.01) in both pyruvate group (PYR) and placebo group (PLA). Compared to PLA, the blood pH, HCO3- and BE were significantly improved in PYR at pre-HIIE (p < 0.01), post-HIIE (p < 0.01) and pre-RSE (p < 0.01). Furthermore, blood BE remained higher in PYR than PLA till end of RSE (p < 0.05). The contribution of oxidative system in the fourth bout of HIIE was higher in PYR than PLA (p < 0.05). In PLA, the ratio of total anaerobic energy contribution during HIIE was higher than that of aerobic (oxidative) (p < 0.01), but not in PYR (p > 0.05). Relative peak power (RPP) of first, fifth sprint, relative average power (RAP) of fifth sprint, the average of RPP and RAP during RSE were significantly improved in PYR compared with PLA (p < 0.05). While no significant changes in the PD% of each bout (p > 0.05) or average PD% (p > 0.05) were observed between the two groups. Conclusion: Pyruvate supplementation for 1-week enhances oxidative system energy contribution and buffers metabolic acidosis during HIIE, and improves RSE performance in acidosis.

ERRATA

PEDIATRICS ◽  
1980 ◽  
Vol 65 (5) ◽  
pp. 1006-1006
Keyword(s):  
Metabolic Acidosis ◽  
Diagnostic Approach ◽  
Acid Base ◽  
Arterial Blood ◽  
Blood Ph ◽  
P 351 ◽  
Normal Acid

In the article "A Diagnostic Approach to Metabolic Acidosis in Children" by Kappy and Morrow (Pediatrics 65:351-356, 1980) on p 351 under "Normal Acid-Base Physiology" the normal arterial blood pH is maintained at 7.40 (H+ = 39.8 nEq/liter not mEq/liter.

The Ventilatory Response in Severe Metabolic Acidosis

1976 ◽  
Vol 50 (5) ◽  
pp. 367-373 ◽  
Author(s):  
M. Fulop
Keyword(s):  
Metabolic Acidosis ◽  
Ventilatory Response ◽  
Acute Hypoxia ◽  
Carbon Dioxide Tension ◽  
Pulmonary Insufficiency ◽  
Plasma Lactate ◽  
Severe Metabolic Acidosis ◽  
Arterial Blood ◽  
Blood Ph ◽  
Insufficient Time

1. The ventilatory response to severe metabolic acidosis was studied by measuring arterial blood carbon dioxide tension and pH in sixty-seven patients with blood pH < 7·10, none of whom had hypercapnia, pulmonary oedema, or chronic pulmonary insufficiency. The results were compared with those previously found in patients with uncomplicated diabetic ketoacidosis. 2. By that comparison, fifty-two of the sixty-seven patients with blood pH < 7·10 were judged to have ‘appropriate hypocapnia’, and fifteen had ‘submaximal hypocapnia’. Thirteen of the latter fifteen had circulatory failure and/or acute hypoxia, and seven of nine in whom it was measured had plasma lactate >9 mmol/l. 3. Hyperventilation was therefore usually well sustained in these patients with severe metabolic acidosis, except in most of those with acute tissue hypoxia. The latter may have had insufficient time to achieve maximum hyperventilation in response to their acidosis, or perhaps their submaximal hypercapnia presaged imminent failure of the hyperventilatory response.

scholarly journals PENDEKATAN STEWART DALAM pH DARAH YANG MENDASARI ASIDOSIS METABOLIK

2018 ◽  
Vol 19 (2) ◽  
pp. 79
Author(s):  
Efrida Efrida ◽  
Ida Parwati ◽  
Ike Sri Redjeki
Keyword(s):  
Metabolic Acidosis ◽  
Ph Value ◽  
Total Concentration ◽  
Ph Measurement ◽  
Strong Ion Difference ◽  
Cross Sectional ◽  
Stewart Approach ◽  
Blood Ph ◽  
Base Disorder ◽  
The Mean

Metabolic acidosis is the most frequent acid-base disorder in patients of the Intensive Care Unit. By conventional approach based onpH value, [HCO3–], and base deficit (BD) from blood gas analyzer (BGA) measurement are often inappropriate with the clinical stateand inadequate in explaining the mechanism of the metabolic acidosis. The Stewart approach states that the blood pH is determinedby a strong ion difference (SID), the carbon dioxide tension (pCO2), the total concentration of non-volatile weak acid. The Stewartapproach may give a better understanding of the mechanisms that underlie the metabolic acidosis. The purpose of this study is to knowthe correlation of blood pH value measurement from BGA and calculation based on Stewart approach and identifying the mechanismsthat underlie a metabolic acidosis. In this study an analytic observational cross-sectional method was used. The examined subjectsconsisted of 71 patients who were admitted with a metabolic acidosis at the ICU from July up to August 2007. All patients were measuredfor their blood pH, pCO2, [HCO3–], BD, sodium, potassium, calcium, magnesium, chloride, lactate, albumin, and phosphate. The resultwas reported as the mean and standard deviation. The data were analyzed by Pearson’s correlation test and linier multiple regression.Statistical significance was determined at p < 0.05. The mean values of blood pH measurement from BGA and blood pH calculationbased on the Stewart approach were 7.33 (0.11) and 7.49 (0.11) (r = 0.681; p < 0.001). Most patients had two underlying mechanisms ofmetabolic acidosis. Hyperlactatemia was present in 61.8%, hyperchloremia was present in 58.2% of patients. Based on this study so far,by using the Stewart approach there is an excellent and significant correlation between the blood pH measurement from BGA and bloodpH calculation. Hyperlactatemia and hyperchloremia are the main causes of the metabolic acidosis in patients of the ICU ward.

Brain pH in acute isocapnic metabolic acidosis and hypoxia: a 31P-nuclear magnetic resonance study

1990 ◽  
Vol 258 (1) ◽  
pp. F34-F40
Author(s):  
S. Adler ◽  
V. Simplaceanu ◽  
C. Ho
Keyword(s):  
Nuclear Magnetic Resonance ◽  
Metabolic Acidosis ◽  
Magnetic Resonance ◽  
Nuclear Magnetic Resonance Study ◽  
Base Change ◽  
Acid Base ◽  
Blood Ph ◽  
31P Nuclear Magnetic Resonance ◽  
Brain Ph ◽  
Nuclear Magnetic

It is well known that brain pH changes rapidly in acute hypercapnia or hypocapnia. The effect of acute isocapnic metabolic acid-base change on brain pH is less certain. To study this problem, acute isocapnic metabolic acidosis was induced by HCl or lactic acid infusions in rats, and recovery from acidosis was accomplished by NaHCO3 infusion. Brain pH was measured by 31P-nuclear magnetic resonance. Despite decreases in blood pH of 0.34 and 0.36 units, respectively, in less than 1 h of acid infusion and rapid recovery during bicarbonate infusion, brain pH was unaffected (ranging between 7.08 and 7.11) and was uncorrelated with blood pH. The blood pH minus brain pH gradient was eliminated by the acidosis. By contrast, hypoxia-induced endogenous lactic acidosis lowered blood and brain pH equivalently, but the fall in brain pH preceded that in blood. During normoxic recovery, brain pH overshot and became alkaline when blood pH was still significantly reduced and blood lactate levels were markedly elevated. Presumably, this is due to stimulated active H+ transport. The results demonstrate that brain pH is affected differently in metabolic, respiratory, and endogenous acid-base disturbances. Thus brain pH cannot be predicted solely from blood pH values.

31P-NMR in vivo measurement of renal intracellular pH: effects of acidosis and K+ depletion in rats

1986 ◽  
Vol 251 (5) ◽  
pp. F904-F910 ◽  
Author(s):  
W. R. Adam ◽  
A. P. Koretsky ◽  
M. W. Weiner
Keyword(s):  
Metabolic Acidosis ◽  
Intracellular Ph ◽  
Respiratory Acidosis ◽  
Resonance Spectroscopy ◽  
Ph Effects ◽  
Potassium Depletion ◽  
Chronic Metabolic Acidosis ◽  
Arterial Blood ◽  
Blood Ph

Renal intracellular pH (pHi) was measured in vivo from the chemical shift (sigma) of inorganic phosphate (Pi), obtained by 31P-nuclear magnetic resonance spectroscopy (NMR). pH was calculated from the difference between sigma Pi and sigma alpha-ATP. Changes of sigma Pi closely correlated with changes of sigma monophosphoesters; this supports the hypothesis that the pH determined from sigma Pi represents pHi. Renal pH in control rats was 7.39 +/- 0.04 (n = 8). This is higher than pHi of muscle and brain in vivo, suggesting that renal Na-H antiporter activity raises renal pHi. To examine the relationship between renal pH and ammoniagenesis, rats were subjected to acute (less than 24 h) and chronic (4-7 days) metabolic acidosis, acute (20 min) and chronic (6-8 days) respiratory acidosis, and dietary potassium depletion (7-21 days). Acute metabolic and respiratory acidosis produced acidification of renal pHi. Chronic metabolic acidosis (arterial blood pH, 7.26 +/- 0.02) lowered renal pHi to 7.30 +/- 0.02, but chronic respiratory acidosis (arterial blood pH, 7.30 +/- 0.05) was not associated with renal acidosis (pH, 7.40 +/- 0.04). At a similar level of blood pH, pHi was higher in chronic metabolic acidosis than in acute metabolic acidosis, suggesting an adaptive process that raises pHi. Potassium depletion (arterial blood pH, 7.44 +/- 0.05) was associated with a marked renal acidosis (renal pH, 7.17 +/- 0.02). There was a direct relationship between renal pH and cardiac K+. Rapid partial repletion with KCl (1 mmol) significantly increased renal pHi from 7.14 +/- 0.03 to 7.31 +/- 0.01.(ABSTRACT TRUNCATED AT 250 WORDS)

Effect of metabolic acidosis on the PTH receptor-adenylate cyclase system of canine kidney

1985 ◽  
Vol 249 (4) ◽  
pp. F566-F572
Author(s):  
E. Bellorin-Font ◽  
J. Humpierres ◽  
J. R. Weisinger ◽  
C. L. Milanes ◽  
V. Sylva ◽  
...  
Keyword(s):  
Enzyme Activity ◽  
Metabolic Acidosis ◽  
Adenylate Cyclase ◽  
Receptor Binding ◽  
Binding Capacity ◽  
Cyclase Activity ◽  
Adenylate Cyclase Activity ◽  
Adenylate Cyclase System ◽  
Serum Bicarbonate ◽  
Blood Ph

The phosphaturic action of parathyroid hormone (PTH) is blunted during metabolic acidosis. Previous studies suggest that the activation of renal cortical adenylate cyclase by PTH is decreased under this condition. However, the mechanisms underlying the defect are not completely defined. The present studies were designed to examine the interaction of PTH with its receptor-adenylate cyclase system in basolateral cortical membranes from dogs with metabolic acidosis. Chronic metabolic acidosis was induced in seven normal dogs. Venous blood pH decreased to 7.21 +/- 0.01 and serum bicarbonate to 12.58 +/- 0.32 meq/liter. In seven control dogs blood pH was 7.38 +/- 0.002 and serum bicarbonate was 20.14 +/- 0.26 meq/liter. The kidneys were surgically removed and basolateral membranes were prepared by differential centrifugation and ultracentrifugation in discontinuous sucrose density gradients for studies of adenylate cyclase activity and hormone-receptor binding. Metabolic acidosis resulted in a significant decrease in PTH-dependent adenylate cyclase activity (Vmax 2,119 +/- 150 pmol cAMP X mg prot-1 .30 min-1 vs. 3,548 +/- 116 in the controls). The PTH concentration giving half-maximal activation of adenylate cyclase was unchanged. However, PTH-receptor binding showed similar affinity and binding capacity in both groups of membranes. Basal enzyme activity was also similar. In the presence of the GTP analogue 5'-guanylylimidodiphosphate, PTH-dependent adenylate cyclase activity remained markedly decreased in the acidotic dog membranes compared with the controls. The ability of NaF to stimulate enzyme activity was also depressed in the membrane of acidotic dogs. Enzyme activity in the presence of Mn2+ was similar in the two groups.(ABSTRACT TRUNCATED AT 250 WORDS)

Possible involvement of somatolactin in the regulation of plasma bicarbonate for the compensation of acidosis in rainbow trout

1997 ◽  
Vol 200 (21) ◽  
pp. 2675-2683
Author(s):  
S Kakizawa ◽  
A Ishimatsu ◽  
T Takeda ◽  
T Kaneko ◽  
T Hirano
Keyword(s):  
Rainbow Trout ◽  
Metabolic Acidosis ◽  
Respiratory Acidosis ◽  
Pituitary Hormone ◽  
Similar Extent ◽  
Acid Infusion ◽  
Control Value ◽  
Rainbow Trout Oncorhynchus Mykiss ◽  
Blood Ph ◽  
The Difference

Somatolactin is a putative pituitary hormone of the growth hormone/prolactin family in fish. Its function is still unknown. The effects of environmental hypercapnia and hypoxia, acid (HCl) infusion and exhaustive exercise on plasma somatolactin levels were examined in the chronically cannulated rainbow trout to study the possible physiological roles of somatolactin. Respiratory acidosis induced by hypercapnia (2% CO2) did not affect plasma somatolactin level. In contrast, metabolic acidosis induced by acid infusion and exercise increased plasma somatolactin level. Blood pH was depressed to a similar extent by both types of acidosis, whereas plasma [HCO3-] was elevated by respiratory acidosis but reduced by metabolic acidosis. A moderate hypoxia (water PO2 9.3kPa) affected neither acid&shy;base status nor plasma somatolactin level. A more severe hypoxia (water PO2 6.1kPa) resulted in metabolic acidosis accompanied by an apparent rise in plasma somatolactin level, although the difference in somatolactin level from the control value was not statistically significant. Somatolactin immunoneutralization retarded recovery of plasma [HCO3-] following acid infusion. These results indicate that somatolactin is involved in the retention of HCO3- during metabolic acidosis but not in the active accumulation of HCO3- for acid&shy;base compensation of respiratory acidosis in rainbow trout Oncorhynchus mykiss.

Intracellular Buffering in the Dog at Varying CO2 Tensions

1972 ◽  
Vol 42 (3) ◽  
pp. 311-324 ◽  
Author(s):  
J. L. Gamble ◽  
P. J. Zuromskis ◽  
J. A. Bettice ◽  
R. L. Ginsberg
Keyword(s):  
Metabolic Acidosis ◽  
Stroke Volume ◽  
Intracellular Ph ◽  
Concentration Gradient ◽  
Significant Interaction ◽  
Cell Membranes ◽  
Mineral Acid ◽  
Extracellular Ph ◽  
Ion Concentration ◽  
Respiratory Change

1. The effect of varying the Pco2 on the buffering of mineral acid has been investigated. HCl (6 mmol/kg) was infused into anaesthetized-paralysed dogs maintained on a respirator and changes in Pco2 (between 20 and 60 mmHg) were arranged by varying the stroke volume. 2. No significant interaction between buffering of respiratory and metabolic events was discerned. Variations in Pco2 did not alter the efficiency of the buffering of the HCl. The presence or absence of metabolic acidosis did not alter the magnitude of the effect of acute respiratory change on the concentration of extracellular bicarbonate. This response remained between 1·0 and 1·3 mmol/l for changes of 10 mmHg in the Pco2. 3. The buffering of HCl achieved outside the blood and extracellular fluids did not correlate with measured changes in extracellular pH or with predicted changes in intracellular pH. This buffering appears to be associated with changes in the H+ ion concentration gradient across the cell membranes.

Effect of metabolic acidosis on proximal tubular total CO2 absorption

1985 ◽  
Vol 249 (1) ◽  
pp. F62-F68 ◽  
Author(s):  
R. T. Kunau ◽  
J. I. Hart ◽  
K. A. Walker
Keyword(s):  
Metabolic Acidosis ◽  
Proximal Tubule ◽  
Brush Border Membrane ◽  
Membrane Vesicles ◽  
Co2 Absorption ◽  
Arterial Blood ◽  
Blood Ph ◽  
In Series ◽  
Proximal Tubular

In vivo microperfusion studies of the proximal convoluted tubule of the rat were performed to determine the effect of metabolic acidosis on total CO2 (tCO2) absorption. In series I, tubular perfusion was performed in control and acidotic rats in a manner by which similar mean total CO2 concentrations in the proximal tubule were maintained. Comparable ranges of perfusion rate were studied in both groups. Following 3 days of HCl ingestion, plasma tCO2 was 20.0 +/- 0.9 mM in the acidotic rats whereas it was 29.6 +/- 0.53 mM in control rats. The arterial blood pH values were 7.25 +/- 0.02 vs. 7.43 +/- 0.01. Starting tCO2 perfusate concentrations were identical in both groups, 29.3 and 29.7 mM, as were the concentrations at the end of the perfused segments, 21.2 and 21.9 mM. The absorption of tCO2 (JtCO2, pmol X mm-1 X min-1) was significantly greater in the acidotic rats than in the controls, 576 +/- 39 vs. 256 +/- 21. At all perfusion rates studied, proximal tubular JtCO2 was higher in the acidotic than in the control rats. In series II, similar lengths of the late proximal tubule were perfused at the same rate in control and acidotic rats. Again, JtCO2 was higher in the acidotic rats, 352 +/- 19 vs. 198 +/- 13. The results indicate that at comparable luminal tCO2 concentration and tubular fluid flow rates, tCO2 absorption is significantly increased in the acidotic state. Although other mechanisms cannot be excluded, the finding of an increase in proximal tCO2 absorption in the acidotic rats is in agreement with the presence of an accelerated Na+/H+ exchange rate in brush border membrane vesicles obtained from the renal cortex of animals with metabolic acidosis.

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