Effects of Intra- and Extracellular Carbonic Anhydrase on CO2 Excretion and Intravascular pH Equilibrium in the Isolated Perfused Rat Lung

2015 ◽  
pp. 26-29 ◽  
Author(s):  
C. Geers ◽  
T. A. Heming ◽  
G. Gros ◽  
A. Bidani ◽  
E. D. Crandall
Keyword(s):  
Carbonic Anhydrase ◽  
Rat Lung ◽  
Co2 Excretion

Roles of intra- and extracellular carbonic anhydrase in alveolar-capillary CO2 equilibration

1994 ◽  
Vol 77 (2) ◽  
pp. 697-705 ◽  
Author(s):  
T. A. Heming ◽  
E. K. Stabenau ◽  
C. G. Vanoye ◽  
H. Moghadasi ◽  
A. Bidani
Keyword(s):  
Carbonic Anhydrase ◽  
Driving Forces ◽  
Excretion Rate ◽  
Blood Gas ◽  
Gas Barrier ◽  
Arterial Pco2 ◽  
Co2 Diffusion ◽  
Chemical Equilibration ◽  
Co2 Excretion ◽  
Alveolar Capillary

Alveolar-capillary CO2 equilibration involves diffusive equilibration of CO2 across the blood-gas barrier and chemical equilibration of perfusate CO2-HCO-3-H+ reactions. These processes are governed by different, but related, driving forces and conductances. The present study examined the importance of pulmonary carbonic anhydrase (CA) for diffusive and reactive CO2 equilibration in isolated rat lungs. Lungs were perfused with salines containing membrane-impermeant or -permeant inhibitors of CA. Measurements of CO2 excretion rate, equilibrated venous and arterial PCO2 and pH, and postcapillary pH and PCO2 disequilibria were used, together with our previous model of CO2-HCO-3-H+ reactions and transport in saline-perfused capillaries (Bidani et al. J. Appl. Physiol. 55: 75–83, 1983), to compute the relevant driving forces and conductances. Reactive CO2 equilibration was markedly affected by extracellular (vascular) CA activity but not by the activity of intracellular (cytosolic) CA. The driving force for CO2 diffusion was strongly influenced by vascular CA activity. The conductance for CO2 diffusion was independent of CA activity. The minimum conductance for CO2 diffusion was estimated to be 700–800 ml.min-1.Torr-1. The results indicate that extracellular vascular CA activity influences both diffusive and reactive CO2 equilibration. However, cytosolic CA has no detectable role in alveolar-capillary CO2 equilibration.

Rat lung carbonic anhydrase: activity, localization, and isozymes

1986 ◽  
Vol 60 (2) ◽  
pp. 638-645 ◽  
Author(s):  
R. P. Henry ◽  
S. J. Dodgson ◽  
R. E. Forster ◽  
B. T. Storey
Keyword(s):  
Enzyme Activity ◽  
Carbonic Anhydrase ◽  
Carbonic Anhydrase Activity ◽  
Hydration Reaction ◽  
Rat Lung ◽  
Cell Debris ◽  
Blood Contamination ◽  
Total Enzyme Activity ◽  
Erythrocyte Lysis ◽  
A Cell

sCarbonic anhydrase activity in rat lungs perfused free of blood was localized by homogenization of the tissue followed by differential centrifugation. Four fractions were obtained from the homogenate, a cell debris pellet with a mitochondrial pellet and a microsomal pellet with a clear cytosol supernatant. The last named fraction contained 67% of the total enzyme activity; the cell debris contained 18%, and the mitochondrial and microsomal contained 8 and 7%, respectively. Of the 33% of enzyme activity associated with the pellet fraction, 25% could be experimentally defined as membrane associated by its solubilization with 0.3 M tris-(hydroxymethyl) aminoethane sulfate buffer. The remainder was defined as membrane bound. Purification of the soluble carbonic anhydrase from the lung yielded two isozymes with electrophoretic and inhibitor sensitivities apparently identical with the blood isozymes. Hemoglobin analysis showed that the lung isozymes could not have included more than 0.03% enzyme from blood contamination. The carbonic anhydrase activity present in the whole rat lung would give an average acceleration of the CO2 hydration reaction under physiological conditions over the uncatalyzed rate of 122, sufficient to maintain equilibration between CO2 and plasma HCO3- during blood transit of the lung. If the membrane-associated activity is mostly on the plasma membrane of the endothelial cells and available to the capillary blood, it would be sufficient to give this acceleration. We suggest that the possible source of this membrane-associated activity might be adsorption from the blood of carbonic anhydrase liberated by erythrocyte lysis.

scholarly journals The pattern of carbon dioxide excretion in the rainbow trout Salmo gairdneri

1978 ◽  
Vol 72 (1) ◽  
pp. 17-24
Author(s):  
M. S. Haswell ◽  
D. J. Randall
Keyword(s):  
Carbon Dioxide ◽  
Rainbow Trout ◽  
Carbonic Anhydrase ◽  
Severe Anaemia ◽  
Salmo Gairdneri ◽  
Gill Epithelium ◽  
Acid Base ◽  
Plasma Bicarbonate ◽  
O2 Delivery ◽  
Co2 Excretion

1. Patterns of carbon dioxide excretion were investigated in rainbow trout (Salmo gairdneri). 2. The loss of erythrocytic carbonic anhydrase caused by severe anaemia does not affect acid/base regulation or the ability of fish to excrete CO2. 3. Bicarbonate excretion across the saline-perfused gills of trout is significant even though residence time for the saline in the gills is only 1--3 s. CO2 excretion across these saline-perfused gills is blocked by the carbonic anhydrase inhibitor, diamox. 4. The excretion of CO2 in fish is via the movement of plasma bicarbonate into the gill epithelium where branchial carbonic anhydrase catalyses the production of CO2. Fish can adjust pH by regulating bicarbonate movement across the gills. 5. The erythrocytic carbonic anhydrase is not necessary for CO2 excretion in the gills but is involved in facilitating Bohr and Root shifts to augment O2 delivery in the tissues.

CO2 excretion and postcapillary pH equilibration in blood-perfused turtle lungs

1999 ◽  
Vol 202 (8) ◽  
pp. 965-975
Author(s):  
E.K. Stabenau ◽  
T.A. Heming
Keyword(s):  
Carbonic Anhydrase ◽  
Anion Exchange ◽  
Cell Suspensions ◽  
Red Cell ◽  
Co2 Partial Pressure ◽  
Arterial Blood ◽  
Pass Perfusion ◽  
Erythrocyte Carbonic Anhydrase ◽  
Co2 Excretion

Turtles possess a significant postcapillary CO2 partial pressure (PCO2) disequilibrium between arterial blood and alveolar gas. There are several possible explanations for this blood disequilibrium including a slow rate of erythrocyte physiological anion shift (Cl-/HCO3- exchange) or inaccessibility of plasma HCO3- to red blood cell or pulmonary carbonic anhydrase. The present study characterized the contribution of erythrocyte anion exchange and pulmonary and erythrocyte carbonic anhydrase to CO2 excretion and, hence, to postcapillary CO2-HCO3--H+ equilibration in blood-perfused turtle (Pseudemys scripta) lungs. Turtle lungs perfused in situ with red cell suspensions containing inhibitors of erythrocyte anion exchange and/or pulmonary and red cell carbonic anhydrase produced significant postcapillary blood PCO2 and pH disequilibria, while no disequilibria were measured when lungs were perfused with control red cell suspensions. Erythrocyte anion exchange and pulmonary intravascular carbonic anhydrase contributed 11 % and 9 %, respectively, to CO2 excretion during single-pass perfusion, whereas red cell and pulmonary carbonic anhydrase contributed 32 % to the measured CO2 excretion. The lack of a measurable PCO2 disequilibrium during perfusion with control erythrocyte suspensions in this study suggests that alternative mechanisms may be responsible for the arterial-lung PCO2 disequilibrium measured during breathing or diving episodes in turtles.

Localization of carbonic anhydrase in the rat lung

1981 ◽  
Vol 72 (3) ◽  
pp. 415-424 ◽  
Author(s):  
N. Sugai ◽  
Y. Ninomiya ◽  
T. Oosaki
Keyword(s):  
Carbonic Anhydrase ◽  
Rat Lung

Blood and Gill Carbonic Anhydrase in the Context of a Chondrichthyan Model of CO2 Excretion

2019 ◽  
Vol 92 (6) ◽  
pp. 554-566 ◽  
Author(s):  
Olivia J. L. McMillan ◽  
Angelina M. Dichiera ◽  
Till S. Harter ◽  
Jonathan M. Wilson ◽  
Andrew J. Esbaugh ◽  
...  
Keyword(s):  
Carbonic Anhydrase ◽  
Co2 Excretion

Pulmonary carbonic anhydrase in the human, monkey, and rat

1982 ◽  
Vol 52 (2) ◽  
pp. 352-356 ◽  
Author(s):  
G. Lonnerholm
Keyword(s):  
Enzyme Activity ◽  
Carbonic Anhydrase ◽  
High Activity ◽  
Lung Tissue ◽  
Close Contact ◽  
Alveolar Epithelium ◽  
Rat Lung ◽  
Alveolar Space ◽  
Co2 Transport ◽  
Pulmonary Capillaries

The distribution of carbonic anhydrase in the human, monkey, and rat lung was studied by the histochemical method of Hansson. High activity of this enzyme was demonstrated in the endothelium of pulmonary capillaries. In the human and the monkey lung enzyme activity was exhibited in the whole circumference of the capillaries, but in the rat enzyme activity is confined to capillary segments having close contact with alveolar epithelium forming the blood-air barrier. Staining was inhibited by 10 microM acetazolamide, but was not affected by 10 microM Cl 13,850, an inactive acetazolamide analogue. The location of carbonic anhydrase in the lung supports the idea that pulmonary carbonic anhydrase promotes CO2 elimination from the blood into the alveolar space. Its possible functions may be to act upon plasma to accelerate the conversion of HCO-3 to CO2 and to facilitate CO2 transport through the lung tissue.

scholarly journals The Role of Carbonic Anhydrase in Respiration, Ion Regulation and Acid-Base Balance in the Aquatic Crab Calunectes Sapidus and the Terrestrial Crab Gecarcinus Lateraus

1983 ◽  
Vol 103 (1) ◽  
pp. 205-223 ◽  
Author(s):  
RAYMOND P. HENRY ◽  
JAMES N. CAMERON
Keyword(s):  
Carbonic Anhydrase ◽  
High Rate ◽  
Elevated Blood ◽  
O2 Uptake ◽  
Acid Base Balance ◽  
Ion Regulation ◽  
Land Crab ◽  
Blood Ph ◽  
Base Balance ◽  
Co2 Excretion

The enzyme carbonic anhydrase (CA), which is concentrated mainly in the osmoregulatory tissue of the gills, appears to be required for ion regulation but not for CO2 excretion. An injection of the CA inhibitor acetazolamide produced an inhibition of between 90 and 100%, which took 6 h to be fully effective, and 48–96 h to wear off. During the period of inhibition in Callinectes sapidus there was no change in either O2 uptake or CO2 excretion, nor was there any increase in blood Pcoco2. In blue crabs acclimated to 250 mosM salinity, at which the animals are ion regulators, inhibition of CA caused both Na+ and Cl− concentrations in the blood to be lowered, with Cl− being lowered to a greater degree. As a result of an increase in the Na+-Cl− difference the animal experienced a ‘metabolic’ alkalosis: elevated blood pH and HCO3− at constant Pco2. The data are consistent with the hypothesis that branchial CA functions in providing H+ and HCO3− as counterions for Na+ and Cl− transport through the hydration of respiratory CO2. In the terrestrial Gecarcinus lateralis, inhibition of CA caused an increase in blood Pco2, but did not alter O2 uptake or CO2 excretion. After an initial acidosis, blood pH and HCO3− increased and remained elevated. Blood osmolality, Na+, Cl− and Ca2+ concentrations all increased, and the animals experienced a high rate of mortality. These data suggest that CA in the land crab is also important in blood ion regulation, probably to combat desiccation.

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