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

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.

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.

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.

Isolated perfused head of rainbow trout. I. Gas transfer, acid-base balance, and hemodynamics

1985 ◽  
Vol 249 (2) ◽  
pp. R246-R254 ◽  
Author(s):  
S. F. Perry ◽  
C. E. Booth ◽  
D. G. McDonald
Keyword(s):  
Carbonic Anhydrase ◽  
Blood Perfusion ◽  
Aortic Pressure ◽  
Gas Transfer ◽  
Acid Base Balance ◽  
Acid Base ◽  
Ph Gradients ◽  
Base Balance ◽  
Co2 Excretion

Branchial gas transfer, acid-base balance, and hemodynamics were critically evaluated and compared in Ringer-perfused and blood-perfused heads of rainbow trout. Blood perfusion stimulated O2 uptake and CO2 excretion across the gills to values more representative of intact fish. The stimulatory effect of blood on gas transfer was due to increased O2 carrying capacity (O2 uptake) and the presence of erythrocytic carbonic anhydrase (CO2 excretion). Adding carbonic anhydrase to Ringer enhanced CO2 excretion in a manner similar to blood. During Ringer perfusion, arteriovenous pH gradients were abnormal (arterial pH less than venous pH). Perfusion with blood or addition of carbonic anhydrase to Ringer reversed the pH gradients to typical in vivo levels. Branchial vascular resistance to flow was abnormally high in both Ringer- and blood-perfused preparations, primarily as a result of low dorsal aortic pressure. Input pressure increased during blood perfusion and was similar to ventral aortic pressure in vivo. Perfusion with Ringer may have caused irreversible deterioration of gill function as indicated by decreased arterial Po2 and O2 extraction effectiveness after a rapid switch from Ringer to blood perfusion. The results are discussed with reference to the suitability of perfused trout head preparations for studying gill gas transfer, acid-base balance, and hemodynamics. Comparisons are made between the perfused head preparation and intact fish as well as with other types of perfused gill preparations.

Effects of dextran-bound inhibitors on carbonic anhydrase activity in isolated rat lungs

1986 ◽  
Vol 61 (5) ◽  
pp. 1849-1856 ◽  
Author(s):  
T. A. Heming ◽  
C. Geers ◽  
G. Gros ◽  
A. Bidani ◽  
E. D. Crandall
Keyword(s):  
Molecular Weight ◽  
Carbonic Anhydrase ◽  
Time Course ◽  
Co2 Concentration ◽  
Carbonic Anhydrase Activity ◽  
Low Molecular Weight ◽  
Co2 Diffusion ◽  
Rat Lungs ◽  
Co2 Excretion ◽  
Isolated Rat

Effects of macromolecular Prontosil-dextran inhibitors (PD) on carbonic anhydrase (CA) activity in isolated rat lungs were studied. Isolated lungs were perfused with Krebs-Ringer bicarbonate (KRB) solutions containing no inhibitor, PD 100,000 (mol wt 100,000), PD 5,000 (mol wt 5,000), or low-molecular-weight inhibitors (Prontosil or acetazolamide). The time course of effluent perfusate pH equilibration was measured in a stop-flow pH electrode apparatus. Pulmonary CO2 excretion (Vco2) was monitored by continuously recording expired CO2 concentration. The lungs were ventilated with room air and perfused at 37 degrees C with KRB prebubbled with 5% CO2- 20% O2- 75% N2. The results obtained show that both the low-molecular-weight inhibitors and PD′s caused postcapillary pH disequilibria (delta pH) in effluent perfusate. However, only acetazolamide and Prontosil caused a reduction in Vco2. These results suggest that there is an intravascular CA, presumably associated with endothelial cell membranes, that is accessible to all inhibitors used and is responsible in part for equilibration of the CO2- HCO3- -H+ reactions in the perfusate but, under the conditions used, does not affect CO2 excretion; and there is an extravascular (possibly intracellular) CA that can be inhibited by low-molecular-weight inhibitors, is primarily responsible for enhanced CO2 transfer across the alveolar-capillary barrier (perhaps via facilitation of CO2 diffusion), and is in part responsible for pH equilibration.

Sensitivity of CO2 excretion to blood flow changes in trout is determined by carbonic anhydrase availability

2002 ◽  
Vol 282 (2) ◽  
pp. R501-R508 ◽  
Author(s):  
Patrick R. Desforges ◽  
Stuart S. Harman ◽  
Kathleen M. Gilmour ◽  
Steve F. Perry
Keyword(s):  
Blood Flow ◽  
Carbonic Anhydrase ◽  
Partial Pressure ◽  
Blood Gases ◽  
Control Fish ◽  
Volume Loading ◽  
Arterial Partial Pressure ◽  
Rainbow Trout Oncorhynchus Mykiss ◽  
Flow Changes ◽  
Co2 Excretion

The blood transit time through the gills of rainbow trout ( Oncorhynchus mykiss) was modified by manipulation of cardiac output (V˙b). The experiments tested the hypothesis that efficiency of CO2 excretion is sensitive to changes in blood flow owing to chemical equilibrium limitations. An extracorporeal blood shunt was used to continuously monitor blood gases in fish in which V˙b was elevated (by 13.3 ± 2.4 ml · min−1 · kg−1) by intravascular saline injection or reduced (by 10.8 ± 1.8 ml · min−1 · kg−1) by removal of plasma. The arterial partial pressure of CO2(PaCO2 ; an index of CO2 excretion efficiency) was increased with elevated V˙b and was decreased with reduced V˙b such that the changes in PaCO2 exhibited a significant positive sigmoidal relationship with the changes in V˙b ( r 2 =0.75; P< 0.05). In contrast, there was no significant relationship between changes in the arterial partial pressure of O2(PaO2 ; an index of O2 uptake efficiency) and changes in V˙b ( r 2 = 0.07; P > 0.05). The intravenous administration of carbonic anhydrase (CA; 10 mg/kg) before vascular volume loading eliminated the increase in PaCO2 with increased V˙b that was observed in control fish.

Membrane-associated carbonic anhydrase in gills of the blue crab, Callinectes sapidus

1987 ◽  
Vol 252 (5) ◽  
pp. R966-R971 ◽  
Author(s):  
R. P. Henry
Keyword(s):  
Carbonic Anhydrase ◽  
Blue Crab ◽  
Callinectes Sapidus ◽  
Rapid Development ◽  
Respiratory Acidosis ◽  
Basal Membrane ◽  
Ion Regulation ◽  
Co2 Excretion

The presence of the enzyme carbonic anhydrase (CA) on the basal membrane of the branchial endothelial cells in the blue crab and its physiological significance were studied in vivo using a membrane-impermeant CA inhibitor, quaternary ammonium sulfanilamide (QAS). Injection of QAS into the hemolymph of Callinectes sapidus resulted in the rapid development of a respiratory acidosis; PCO2 rose almost 2 Torr, pH was lowered by approximately 0.25 units, and total CO2 rose by 2 mM. These results support the hypothesis that membrane-associated CA exposed to hemolymph is present in the crustacean gill and that it is physiologically significant in mobilizing hemolymph HCO-3 to CO2 to facilitate CO2 excretion across the gill. The recovery from this acidosis coincides with the clearance of the inhibitor from the hemolymph. Hemolymph osmotic and ionic parameters were unaffected by QAS, reconfirming the role of branchial cytoplasmic CA in ion regulation and also providing a convenient bioassay for determining CA inhibitor permeability in the intact organism.

Equilibrium of CO2 reactions in the pulmonary capillary

1980 ◽  
Vol 48 (6) ◽  
pp. 972-976 ◽  
Author(s):  
R. A. Klocke
Keyword(s):  
Carbonic Anhydrase ◽  
Enzyme Catalysis ◽  
Production Control ◽  
Co2 Production ◽  
Bovine Carbonic Anhydrase ◽  
Pulmonary Capillary ◽  
Native Lung ◽  
Bicarbonate Solutions ◽  
Co2 Excretion

Steady-state CO2 excretion was measured in isolated blood-free rabbit lungs perfused with bicarbonate solutions. CO2 in the expired ventilation was either present initially in the perfusate as dissolved CO2 or produced from bicarbonate during pulmonary capillary transit. The two components were separated by measurement of simultaneous acetylene excretion. Bovine carbonic anhydrase and acetazolamide were sequentially added to the perfusate to determine the effects of maximal enzyme catalysis and inhibition of native lung carbonic anhydrase on CO2 production. Control CO2 production was significantly greater than that observed during inhibition of native lung carbonic anhydrase, confirming previous observations that bicarbonate has access to the tissue enzyme. Addition of excess carbonic anhydrase increased CO2 production by a statistically, but not physiologically, significant amount. These data demonstrate that CO2 reactions outside the erythrocyte attain 97% completion during pulmonary capillary transit. Under control and catalyzed conditions, alveolar and venous CO2 tens ions and pH were essentially identical to equilibrium values determined by in vitro tonometry.

Sign in / Sign up

Export Citation Format

Share Document