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.

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.

Airway vasodilation by bradykinin is mediated via B2 receptors and modulated by peptidase inhibitors

1994 ◽  
Vol 266 (2) ◽  
pp. L156-L162
Author(s):  
I. Yamawaki ◽  
P. Geppetti ◽  
C. Bertrand ◽  
B. Chan ◽  
J. A. Nadel
Keyword(s):  
Blood Flow ◽  
Left Ventricle ◽  
Angiotensin Converting Enzyme ◽  
Reference Sample ◽  
Neutral Endopeptidase ◽  
Converting Enzyme ◽  
B1 Receptor ◽  
Bradykinin B1 Receptor ◽  
B2 Receptors

We studied the effect of exogenous bradykinin on blood flow in the airway microcirculation of anesthetized F344 rats in vivo. We made three successive determinations of airway blood flow and cardiac output using a modification of the reference sample microsphere technique. Injection of bradykinin into the left ventricle increased airway blood flow in a dose-related manner. Pretreatment with the bradykinin B2 receptor antagonist, Hoe 140, completely abolished bradykinin-, but not histamine-induced vasodilation. A bradykinin B1 receptor agonist, [des-Arg9]bradykinin, did not affect airway blood flow. We also studied the effect of inhibitors of angiotensin-converting enzyme (captopril) and neutral endopeptidase (phosphoramidon) on bradykinin-induced vasodilation. Pretreatment with captopril, but not phosphoramidon, potentiated the bradykinin-induced vasodilation. However, the addition of phosphoramidon further potentiated the effect of captopril. We conclude that injection of bradykinin into the left ventricle produces a dose-related vasodilation in the airway microcirculation mediated via B2 receptors, an effect that is modulated primarily by angiotensin-converting enzyme and, to a lesser extent, by neutral endopeptidase.

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.

Effects of alveolar pressure on lung angiotensin-converting enzyme function in vivo

1986 ◽  
Vol 61 (3) ◽  
pp. 1041-1050 ◽  
Author(s):  
H. J. Toivonen ◽  
J. D. Catravas
Keyword(s):  
Mechanical Ventilation ◽  
Blood Flow ◽  
Angiotensin Converting Enzyme ◽  
Pulmonary Blood Flow ◽  
Enzyme Function ◽  
Luminal Surface ◽  
Converting Enzyme ◽  
Alveolar Pressure ◽  
Indirect Measure

Angiotensin-converting enzyme lines the luminal surface of pulmonary capillary endothelial cells. The metabolism of its synthetic substrate, 3H-benzoyl-L-phenylalanyl-L-alanyl-L-proline ([3H]BPAP) has been used as an indicator of pulmonary microvascular function. Because the flow-volume status of the pulmonary capillaries is dependent on intra-alveolar pressure, we have studied the effects of airway pressure on endothelial plasmalemmal angiotensin-converting enzyme function in rabbit lungs in vivo. Static inflation of the lungs to a pressure of 0 or 5 Torr did not change percent transpulmonary metabolism and Amax/Km ratio (defined as E X Kcat/Km and thus, under normal conditions, an indirect measure of perfused endothelial luminal surface area) compared with control measurements during conventional mechanical ventilation. When the inflation pressure was increased to 10 Torr, percent metabolism of [3H]BPAP remained unaltered but Amax/Km decreased to 60% of the control value. This decrease was in close relation to the decrease in pulmonary blood flow. Addition of 5 cmH2O positive end-expiratory pressure (PEEP) to the mechanical ventilation also decreased Amax/Km values and pulmonary blood flow but did not influence percent metabolism of [3H]BPAP. These results suggest that the detected alterations in apparent enzyme kinetics were more likely due to hemodynamic changes than to alterations in angiotensin-converting enzyme function. Thus high static alveolar pressures as well as PEEP probably reduced the fraction of perfused microvessels as reflected in changes in Amax/Km ratios. This information should prove useful in interpreting the response of pulmonary endothelial enzymes to injury.

Evidence of active regulation of cerebrospinal fluid acid-base balance

1981 ◽  
Vol 51 (2) ◽  
pp. 369-375 ◽  
Author(s):  
S. W. Bledsoe ◽  
D. Y. Eng ◽  
T. F. Hornbein
Keyword(s):  
Cerebrospinal Fluid ◽  
Electrical Potential ◽  
Respiratory Acidosis ◽  
Respiratory Alkalosis ◽  
Electrical Potential Difference ◽  
Passive Transport ◽  
Acid Base Balance ◽  
Acid Base ◽  
Transport Control ◽  
Base Balance

To test the passive transport hypothesis of cerebrospinal fluid (CSF) [H+] regulation, we altered the relationship between plasma [H+] and the electrical potential difference between CSF and blood (PD) by elevating plasma [K+] during 6-h systemic acid-base disturbances. In five groups of pentobarbital-anesthetized dogs, we increased plasma [K+] from 3.5 to an average of 7.8 meq/l. Hyperkalemia produced an increase in the PD of 6.3 mV by 6 h with normal plasma acid-base status (pHa 7.4), of 8.3 mV with isocapnic metabolic acidosis (pHa 7.2), of 5.3 mV with isocapnic metabolic alkalosis (pHa 7.6), of 9.2 mV with isobicarbonate respiratory acidosis (PaCO2 61 Torr) and of 5.7 mV with isobicarbonate respiratory alkalosis (PaCO2 25 Torr). The change in CSF [H+] at 6 h in each group was the same as that observed in normokalemic animals (Am. J. Physiol. 228: 1134-1154, 1975). This result is not consistent with the passive transport hypothesis. The CSF-blood PD is therefore not an important determinant of CSF [H+] CSF [H+] homeostasis must result from some form of active transport control.

scholarly journals Metabolic component of intestinal Pco 2during dysoxia

2000 ◽  
Vol 89 (6) ◽  
pp. 2422-2429 ◽  
Author(s):  
Ovais Raza ◽  
Robert Schlichtig
Keyword(s):  
Blood Flow ◽  
Carbonic Acid ◽  
Respiratory Acidosis ◽  
Tissue Fluid ◽  
Acid Base Balance ◽  
Acid Base ◽  
First Order Kinetics ◽  
Base Balance ◽  
Buffer Base ◽  
Made In

The adequacy of intestinal perfusion during shock and resuscitation might be estimated from intestinal tissue acid-base balance. We examined this idea from the perspective of conventional blood acid-base physicochemistry. As the O2 supply diminishes with failing blood flow, tissue acid-base changes are first “respiratory,” with CO2 coming from combustion of fuel and stagnating in the decreasing blood flow. When the O2supply decreases to critical, the changes become “metabolic” due to lactic acid. In blood, the respiratory vs. metabolic distinction is conventionally made using the buffer base principle, in which buffer base is the sum of HCO3 − and noncarbonate buffer anion (A−). During purely respiratory acidosis, buffer base stays constant because HCO3 − cannot buffer its own progenitor, carbonic acid, so that the rise of HCO3 − equals the fall of A−. During anaerobic “metabolism,” however, lactate's H+ is buffered by both A− and HCO3 −, causing buffer base to decrease. We quantified the partitioning of lactate's H+ between HCO3 − and A−buffer in anoxic intestine by compressing intestinal segments of anesthetized swine into a steel pipe and measuring Pco 2 and lactate at 5- to 10-min intervals. Their rises followed first-order kinetics, yielding k = 0.031 min−1 and half time = ∼22 min. Pco 2 vs. lactate relations were linear. Over 3 h, lactate increased by 31 ± 3 mmol/l tissue fluid (mM) and Pco 2 by ∼17 mM, meaning that one-half of lactate's H+ was buffered by tissue HCO3 − and one-half by A−. The data were consistent with a lumped p K a value near 6.1 and total A− concentration of ∼30 mmol/kg. We conclude that the respiratory vs. metabolic distinction could be made in tissue by estimating tissue buffer base from measured pH and Pco 2.

Changes in acid-base balance of chick embryos exposed to a He or SF6 atmosphere

1981 ◽  
Vol 50 (4) ◽  
pp. 819-823 ◽  
Author(s):  
H. Tazawa ◽  
J. Piiper ◽  
A. Ar ◽  
H. Rahn
Keyword(s):  
Chick Embryo ◽  
Respiratory Acidosis ◽  
Respiratory Alkalosis ◽  
Chick Embryos ◽  
Acid Base Balance ◽  
Acid Base ◽  
Ph Changes ◽  
Base Balance

On day 16 of the chick embryo, a catheter was implanted in the allantoic vein carrying arterialized blood, and a syringe was attached to the blunt end of the shell connecting to the air cell. This technique allowed for repetitive sampling and analysis of air cell gas and arterialized blood when these eggs were exposed to a He-O2 or SF6-O2 atmosphere. Exposure to He-O2 reduced the arterial CO2 tension(PaCO2) from 36 to 17 Torr and increased pH by 0.17 units; exposure to SF6-O2 increased PaCO2 from 37 to 62 Torr and reduced the pH by 0.14 units. These responses were brought about by changes in the gas conductance of the shell, resulting in a diffusive hypocapnia and respiratory alkalosis in He-O2 and a diffusive hypercapnia and respiratory acidosis in SF6-O2. During a 4-h exposure to these foreign gases the observed pH changes were smaller than predicted because of marked shifts of HCO3- into the blood (SF6-O2) or out of the blood (He-O2).

EXHAUSTIVE EXERCISE IN THE SEA LAMPREY (PETROMYZON MARINUS): RELATIONSHIP BETWEEN ANAEROBIC METABOLISM AND INTRACELLULAR ACID-BASE BALANCE

1993 ◽  
Vol 178 (1) ◽  
pp. 71-88 ◽  
Author(s):  
R. G. Boutilier ◽  
R. A. Ferguson ◽  
R. P. Henry ◽  
B. L. Tufts
Keyword(s):  
Respiratory Acidosis ◽  
High Energy ◽  
Exhaustive Exercise ◽  
Acid Base Balance ◽  
Acid Base ◽  
Ph Change ◽  
Lactate Dehydrogenase Activity ◽  
Base Balance ◽  
Intracellular Acid

We measured intracellular acid-base balance and indicators of carbohydrate and high-energy phosphate metabolism as lampreys recovered from exhaustive exercise. A combined respiratory and metabolic acidosis was observed in the locomotory muscle following ‘burst’ exercise. Muscle pH decreased from approximately 7.2 to 6.7, whereas intracellular PCO2 rose from approximately 0.6 to 1.6 kPa. Unlike the situation in similarly stressed teleost fish such as rainbow trout, the respiratory acidosis in muscle persisted for several hours. This apparent CO2 retention in lamprey muscle may be the result of a restricted ability of the circulatory system to transport CO2 due to reduced erythrocyte anion exchange, or it could represent a restricted ability of the muscle itself to clear the intracellular pool of CO2 due to reduced carbonic anhydrase activity. Maximal lactate dehydrogenase activity of lamprey muscle exhibited a marked dependence on pH, increasing in activity by 30 % as pH decreased from 7.2 to 6.7 (reflecting the ‘resting’ to ‘post- exercise’ pH change observed in vivo). Following exhaustive exercise, the acid-base balance of the muscle is influenced by both proton- consuming (e.g. AMP deamination, glycogen replenishment) and proton-producing (e.g. rephosphorylation of creatine) metabolic processes. The net effect is that, although intracellular pH is maximally depressed, energy stores such as phosphocreatine and glycogen are partially restored within 1 h of exhaustive exercise, placing the animal in good stead for further locomotory work.

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