The effects of respiratory alkalosis and acidosis on net bicarbonate flux along the rat loop of Henle in vivo

1997 ◽  
Vol 273 (5) ◽  
pp. F698-F705
Author(s):  
R. Unwin ◽  
R. Stidwell ◽  
S. Taylor ◽  
G. Capasso
Keyword(s):  
Respiratory Acidosis ◽  
Respiratory Alkalosis ◽  
Loop Of Henle ◽  
Transport Mechanisms ◽  
Bicarbonate Concentration ◽  
Acid Base ◽  
Blood Ph ◽  
Tubule Lumen ◽  
Flux Formula

We have studied the effects of acute respiratory alkalosis (ARALK, hyperventilation) and acidosis (ARA, 8% CO2), chronic respiratory acidosis (CRA; 10% CO2 for 7–10 days), and subsequent recovery from CRA breathing air on loop of Henle (LOH) net bicarbonate flux ([Formula: see text]) by in vivo tubule microperfusion in anesthetized rats. In ARALK blood, pH increased to 7.6, and blood bicarbonate concentration ([[Formula: see text]]) decreased from 29 to 22 mM. Fractional urinary bicarbonate excretion ([Formula: see text]) increased threefold, but LOH[Formula: see text]was unchanged. In ARA, blood pH fell to 7.2, and blood [[Formula: see text]] rose from 28 to 34 mM; [Formula: see text] was reduced to <0.1%, but LOH[Formula: see text]was unaltered. In CRA, blood pH fell to 7.2, and blood [[Formula: see text]] increased to >50 mM, whereas[Formula: see text]decreased to <0.1%.[Formula: see text]was reduced by ∼30%. Bicarbonaturia occurred when CRA rats breathed air, yet LOH[Formula: see text]increased (by 30%) to normal. These results suggest that LOH[Formula: see text]is affected by the blood-to-tubule lumen [[Formula: see text]] gradient and[Formula: see text] backflux. When the usual perfusing solution at 20 nl/min was made[Formula: see text] free, mean[Formula: see text]was −34.5 ± 4.4 pmol/min compared with 210 ± 28.1 pmol/min plus [Formula: see text]. When a low-NaCl perfusate (to minimize net fluid absorption) containing mannitol and acetazolamide (2 × 10−4 M, to abolish H+-dependent[Formula: see text]) was used,[Formula: see text]was −112.8 ± 5.6 pmol/min. Comparable values for[Formula: see text]at 10 nl/min were −35.9 ± 5.8 and −72.5 ± 8.8 pmol/min, respectively. These data indicate significant backflux of[Formula: see text] along the LOH, which depends on the blood-to-lumen [[Formula: see text]] gradient; in addition to any underlying changes in active acid-base transport mechanisms, [Formula: see text]permeability and backflux are important determinants of LOH[Formula: see text]in vivo.

Practical Evaluation of Acid-Base Balance

1957 ◽  
Vol 3 (5) ◽  
pp. 631-637
Author(s):  
Herbert P Jacobi ◽  
Anthony J Barak ◽  
Meyer Beber
Keyword(s):  
Respiratory Acidosis ◽  
Respiratory Alkalosis ◽  
Acid Base Balance ◽  
Bicarbonate Concentration ◽  
Acid Base ◽  
Plasma Bicarbonate ◽  
Practical Evaluation ◽  
Base Balance

Abstract The Co2 combining power bears a variable relationship to the in vivo plasma bicarbonate concentration, depending upon the type and severity of acid-base distortion. In respiratory alkalosis and metabolic acidosis the Co2 combining power will usually be greater than the in vivo plasma bicarbonate concentration; whereas, in respiratory acidosis and metabolic alkalosis the Co2 combining power will usually be less. Co2 content, on the other hand, will always parallel the in vivo plasma bicarbonate concentration quite closely, being only slightly greater. These facts, together with other considerations which are discussed, recommend the abandonment of the determination of CO2 combining power.

The influence of respiratory acid-base changes on muscle performance and excitability of the sarcolemma during strenuous intermittent hand grip exercise

2012 ◽  
Vol 112 (4) ◽  
pp. 571-579 ◽  
Author(s):  
M. Hilbert ◽  
V. Shushakov ◽  
N. Maassen
Keyword(s):  
Force Production ◽  
Respiratory Acidosis ◽  
Respiratory Alkalosis ◽  
Muscle Performance ◽  
Protective Effects ◽  
Acid Base ◽  
M Wave ◽  
Hand Grip

Acidification has been reported to provide protective effects on force production in vitro. Thus, in this study, we tested if respiratory acid-base changes influence muscle function and excitability in vivo. Nine subjects performed strenuous, intermittent hand grip exercises (10 cycles of 15 s of work/45 s of rest) under respiratory acidosis by CO2 rebreathing, alkalosis by hyperventilation, or control. The Pco2, pH, K+ concentration ([K+]), and Na+ concentration were measured in venous and arterialized blood. Compound action potentials (M-wave) were elicited to examine the excitability of the sarcolemma. The surface electromyogram (EMG) was recorded to estimate the central drive to the muscle. The lowest venous pH during the exercise period was 7.24 ± 0.03 in controls, 7.31 ± 0.05 with alkalosis, and 7.17 ± 0.04 with acidosis ( P < 0.001). The venous [K+] rose to similar maximum values in all conditions (6.2 ± 0.8 mmol/l). The acidification reduced the decline in contraction speed ( P < 0.001) but decreased the M-wave area to 73.4 ± 19.8% ( P < 0.001) of the initial value. After the first exercise cycle, the M-wave area was smaller with acidosis than with alkalosis, and, after the second cycle, it was smaller with acidosis than with the control condition ( P < 0.001). The duration of the M-wave was not affected. Acidification diminished the reduction in performance, although the M-wave area during exercise was decreased. Respiratory alkalosis stabilized the M-wave area without influencing performance. Thus, we did not find a direct link between performance and alteration of excitability of the sarcolemma due to changes in pH in vivo.

Acid-base changes in milk and blood of rats in acidosis and alkalosis

1976 ◽  
Vol 231 (1) ◽  
pp. 132-135 ◽  
Author(s):  
R Yagil ◽  
Z Lerner ◽  
Z Etzion ◽  
GM Berlyne
Keyword(s):  
Metabolic Alkalosis ◽  
Respiratory Acidosis ◽  
Bicarbonate Concentration ◽  
Acid Base ◽  
White Rats ◽  
Blood Ph ◽  
Base Parameters ◽  
Acid Base Status ◽  
Heart Blood ◽  
Acute Metabolic Acidosis

Lactating white rats (Rattus norvegicus) were subjected to metabolic and respiratory acidosis and metabolic alkalosis. Before and during the various treatments, the acid-base status of heart blood and milk was determined. Acute metabolic acidosis lowered the pH of plasma and milk; Pco(2) and bicarbonate concentrations in plasma were lowered, and in milk Pco(2) was raised and the bicarbonate concentration remained unchanged. Respiratory acidosis and acetazolamide caused a drop in blood pH and in blood and milk bicarbonate concentrations; milk pH remained unchanged, but Pco(2) was raised in both plasma and milk. Acute metabolic alkalosis raised the blood pH and milk Pco(2); plasma Pco(2) and bicarbonate concentrations in blood and milk remained unchanged. The data show that greater changes occur in acid-base parameters of blood than milk when animals are exposed to acidifying and alkalinizing stimuli.

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

1982 ◽  
Vol 242 (5) ◽  
pp. G486-G492 ◽  
Author(s):  
G. M. Feldman ◽  
A. N. Charney
Keyword(s):  
Sodium Chloride ◽  
Respiratory Alkalosis ◽  
Bicarbonate Secretion ◽  
Sprague Dawley ◽  
Bicarbonate Concentration ◽  
Acid Base ◽  
Plasma Bicarbonate ◽  
Sprague Dawley Rats ◽  
Chloride Absorption

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.

Effects of acid-base imbalance on pulmonary angiotensin-converting enzyme in vivo

1987 ◽  
Vol 63 (4) ◽  
pp. 1629-1637 ◽  
Author(s):  
H. J. Toivonen ◽  
J. D. Catravas
Keyword(s):  
Blood Flow ◽  
Angiotensin Converting Enzyme ◽  
Respiratory Rate ◽  
Airway Pressure ◽  
Respiratory Acidosis ◽  
Respiratory Alkalosis ◽  
Converting Enzyme ◽  
Acid Base Balance ◽  
Acid Base

The effects of acid-base balance disturbances on pulmonary endothelial angiotensin-converting enzyme (ACE) were studied in anesthetized mechanically ventilated rabbits. Enzyme function was estimated from [3H]benzoyl-Phe-Ala-Pro ([3H]BPAP) utilization under first-order reaction conditions during a single transpulmonary passage and expressed as 1) substrate metabolism (M), 2) Amax/Km (Amax being equal to the product of enzyme mass and the constant of product formation), and 3) (Amax/Km)/100 ml blood flow. When respiratory acidosis/alkalosis was produced by altering respiratory rate at constant airway pressure, substrate (BPAP) utilization varied proportionally to arterial pH and inversely proportionally to arterial PCO2 (PaCO2) (P less than 0.05). Percent BPAP metabolism (%M) ranged from 92 +/- 3 (respiratory alkalosis) to 85 +/- 3 (normal), 82 +/- 3 (respiratory acidosis), and 78 +/- 2% (severe respiratory acidosis). Amax/Km similarly decreased from 899 +/- 129 to 825 +/- 143, 601 +/- 74, and 450 +/- 34 ml/min, respectively, and (Amax/Km)/100 ml blood flow was reduced from 176 +/- 26 to 131 +/- 22, 111 +/- 12, and 97 +/- 5, respectively. However, when respiratory acidosis/alkalosis was produced by altering both respiratory rate and airway pressure, no changes were observed in either %M, Amax/Km or (Amax/Km)/100 ml blood flow. Similarly metabolic alkalosis or acidosis did not alter M, Amax/Km or (Amax/Km)/100 ml blood flow. These results indicate that pulmonary endothelial ACE function can be affected by acid-base disturbances, probably indirectly through changes in perfused microvascular surface area.

Role of ion transfer processes in acid-base regulation with temperature changes in fish

1984 ◽  
Vol 246 (4) ◽  
pp. R441-R451 ◽  
Author(s):  
N. Heisler
Keyword(s):  
Ion Transfer ◽  
Bicarbonate Concentration ◽  
Acid Base ◽  
Fish Tissues ◽  
Model Calculations ◽  
Temperature Changes ◽  
Transfer Processes ◽  
Transfer Mechanisms

The contributions of transmembrane and transepithelial ion transfer processes and of nonbicarbonate buffering to the in vivo acid-base regulation have been evaluated. Model calculations were performed utilizing experimental data on transepithelial transfer of ions relevant for the acid-base regulation, the intracellular buffering properties of fish tissues, and the behavior of intracellular and extracellular pH and bicarbonate concentration with changes of temperature. The results of these studies indicate that the changes in the pK values of physiological nonbicarbonate buffers with changes in temperature support the adjustment of pH to lower values with rising temperature; however, transmembrane and transepithelial ion transfer mechanisms determine the acid-base regulation of intracellular and extracellular compartments.

Respiratory Acidosis and Alkalosis

2017 ◽  
Author(s):  
Horacio J Adrogué ◽  
Nicolaos E Madias
Keyword(s):  
Carbonic Acid ◽  
Clinical Manifestations ◽  
Respiratory Acidosis ◽  
Respiratory Alkalosis ◽  
Body Fluids ◽  
The Body ◽  
Acid Base ◽  
Acid Base Equilibrium ◽  
Therapeutic Principles ◽  
The Impact

Respiratory acid-base disorders are those disturbances in acid-base equilibrium that are expressed by a primary change in CO2 tension (Pco2) and reflect primary changes in the body’s CO2 stores (i.e., carbonic acid). A primary increase in Pco2 (and a primary increase in the body’s CO2 stores) defines respiratory acidosis or primary hypercapnia and is characterized by acidification of the body fluids. By contrast, a primary decrease in Pco2 (and a primary decrease in the body’s CO2 stores) defines respiratory alkalosis or primary hypocapnia and is characterized by alkalinization of the body fluids. Primary changes in Pco2 elicit secondary physiologic changes in plasma [HCO3ˉ] that are directional and proportional to the primary changes and tend to minimize the impact on acidity. This review presents the pathophysiology, secondary physiologic response, causes, clinical manifestations, diagnosis, and therapeutic principles of respiratory acidosis and respiratory alkalosis.  This review contains 4 figures, 3 tables, and 59 references. Key words: Respiratory acidosis, respiratory alkalosis, primary hypercapnia, primary hypocapnia, hypoxemia, pseudorespiratory alkalosis

Evaluation of a dual-function pH and PCO2 in vivo sensor

1976 ◽  
Vol 40 (4) ◽  
pp. 625-629 ◽  
Author(s):  
R. L. Coon ◽  
N. C. Lai ◽  
J. P. Kampine
Keyword(s):  
Respiratory Acidosis ◽  
Mean Difference ◽  
Dual Function ◽  
Sodium Pentobarbital ◽  
Trend Monitoring ◽  
Blood Ph ◽  
Arterial Ph ◽  
The Mean ◽  
In Vivo Sensing

A newly developed, dual-function pH and PCO2 sensor was evaluated in this study. The sensors were placed in the femoral arteries of dogs anesthetized with sodium pentobarbital. Comparisons were made between systemic arterial pH and PCO2 measured using the sensor and those measured from blood samples drawn at 15-min intervals over a 7-h period using a bench instrument. The mean pH of the bench instrument measurements was 7.43. The mean difference of the sensor measurements from the bench instrument measurements for 207 comparisons was 0.0003 pH +/- 0.061 SD. The mean PCO2 of the bench instrument measurements was 40 mmHg. The mean difference of the sensor measurements from those of the bench instrument for 212 comparisons was -1.43 mmHg +/- 5.17 SD. The sensors performed equally well in the presence of metabolic or respiratory acidosis and alkalosis. The dual-function sensors evaluated in this study are useful for trend monitoring of pH and PCO2 over at least a 7-h period without recalibration. With improvement in the consistency of sensor construction, these sensors will be reliable in vivo sensing devices for blood pH and PCO2 and thus valuable research and clinical instruments.

Stability of cerebrospinal fluid pH in chronic acid-base disturbances in blood

1965 ◽  
Vol 20 (3) ◽  
pp. 443-452 ◽  
Author(s):  
R. A. Mitchell ◽  
C. T. Carman ◽  
J. W. Severinghaus ◽  
B. W. Richardson ◽  
M. M. Singer ◽  
...  
Keyword(s):  
Metabolic Acidosis ◽  
Active Transport ◽  
Respiratory Acidosis ◽  
Normal Subjects ◽  
Respiratory Alkalosis ◽  
Regulation Of Respiration ◽  
Respiratory Drive ◽  
Acid Base ◽  
Peripheral Chemoreceptors ◽  
Mean Values

In chronic acid-base disturbances, CSF pH was generally within the normal limits (7.30–7.36 units, being the range including two standard deviations of 12 normal subjects). The mean values of CSF and arterial pHH, respectively, were: 1) metabolic alkalosis, 7.337 and 7.523; 2) metabolic acidosis, 7.315 and 7.350; 3) respiratory alkalosis, 7.336 and 7.485; and 4) respiratory acidosis (untreated), 7.314 and 7.382. Other investigators report similar values. The constancy of CSF pH cannot be explained by a poorly permeable blood-CSF barrier in chronic metabolic acidosis and alkalosis, nor can it be explained by respiratory compensation. It cannot be explained by renal compensation in respiratory alkalosis (high altitude for 8 days), although it may be explained by renal compensation in respiratory acidosis. The former three states suggest that active transport regulation of CSF pH is a function of the blood-CSF barrier. Since CSF pH is constant, so also must that portion of the respiratory drive originating in the superficial medullary respiratory chemoreceptors be constant. Ventilation changes in chronic acid-base disturbances thus may result from changes in the activity of peripheral chemoreceptors, in response to changes in arterial pH, arterial PO2, and possibly in neuromuscular receptors. regulation of respiration; medullary respiratory; chemoreceptors; peripheral chemoreceptors; metabolic acidosis and alkalosis; respiratory acidosis and alkalosis; active transport; blood-brain barrier; pregnancy Submitted on July 27, 1964

Relative effects of systemic pH, PCO2, and bicarbonate concentration on ileal ion transport

1983 ◽  
Vol 245 (2) ◽  
pp. G230-G235 ◽  
Author(s):  
A. N. Charney ◽  
L. P. Haskell
Keyword(s):  
Exchange Process ◽  
Respiratory Acidosis ◽  
Electrolyte Transport ◽  
Sodium Absorption ◽  
Sprague Dawley ◽  
Bicarbonate Concentration ◽  
In Situ Perfusion ◽  
Plasma Bicarbonate ◽  
Blood Ph ◽  
Before And After

To determine the relative effects of systemic pH, CO2 tension (PCO2), and bicarbonate concentration on ileal electrolyte transport, states of acute metabolic acidosis and alkalosis were created in Sprague-Dawley rats by gavage feeding (NH4)2SO4 and NaHCO3, respectively. During in situ perfusion of the ileum in anesthetized animals, electrolyte transport was measured before and after respiratory compensation of the systemic pH. Acute respiratory acidosis and alkalosis also were studied by ventilating animals with 0, 3, or 8% CO2. When animals in all groups were considered, net sodium absorption correlated very well with blood pH (r = -0.97). Net bicarbonate secretion correlated with the plasma bicarbonate concentration (r = 0.91) independently of blood pH and PCO2. Net chloride absorption correlated with blood PCO2 (r = 0.92) and was altered when systemic pH and bicarbonate concentration changed in opposite directions. Alterations in luminal pH and PCO2 did not affect electrolyte transport. These results suggest that systemic pH affects a sodium chloride absorptive process and that the plasma bicarbonate concentration affects a chloride absorptive-bicarbonate secretory exchange process in the rat ileum.

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