scholarly journals The distribution of branchial carbonic anhydrase and the effects of gill and erythrocyte carbonic anhydrase inhibition in the channel catfish Ictalurus punctatus

1988 ◽  
Vol 134 (1) ◽  
pp. 201-218 ◽  
Author(s):  
R. P. Henry ◽  
N. J. Smatresk ◽  
J. N. Cameron
Keyword(s):  
Carbonic Anhydrase ◽  
Ictalurus Punctatus ◽  
Channel Catfish ◽  
Time Course ◽  
Respiratory Acidosis ◽  
Transport Processes ◽  
Delay Compensation ◽  
Acid Base ◽  
Acid Base Disturbance ◽  
Erythrocyte Carbonic Anhydrase

Carbonic anhydrase (CA) activity was assayed in lysed erythrocytes and in branchial cytoplasm, mitochondria and microsomes of the channel catfish, Ictalurus punctatus. Branchial CA activity was highest in the cytoplasmic fraction, but activity was very low in mitochondria and microsomes. Erythrocyte CA activity was over four-fold greater than that in the gills. Intact animals were injected with the CA inhibitors acetazolamide and benzolamide. Slow, intra-arterial injection of both inhibitors elicited transient side effects of apnoea, bradycardia and hypoxaemia. Acetazolamide and benzolamide induced a mixed but primarily respiratory acidosis. The onset and the time course of the acidosis were correlated with the inhibition of erythrocyte CA; acetazolamide acted faster because it is more freely diffusible than benzolamide. The acid-base disturbance in the blood reached its maximum after 2 h; compensation was delayed until 24 h, when CA inhibition began to disappear. We conclude from these results that there is very little, if any, membrane-associated CA in the gill, and that the branchial enzyme is not quantitatively important in directly converting plasma HCO3- to CO2 for excretion. Rather, CO2 excretion is accomplished via the traditional chloride shift, followed by intracellular dehydration of HCO3- by erythrocyte CA. These results also suggest that branchial cytoplasmic CA inhibition might impair ion transport processes that are used to compensate blood acid-base disturbances and thus delay compensation of the respiratory acidosis.

Roles of gill and red cell carbonic anhydrase in elasmobranch HCO3- and CO2 excretion

1987 ◽  
Vol 253 (3) ◽  
pp. R450-R458 ◽  
Author(s):  
E. R. Swenson ◽  
T. H. Maren
Keyword(s):  
Carbonic Anhydrase ◽  
Respiratory Acidosis ◽  
Red Cell ◽  
Acid Base ◽  
Terrestrial Vertebrates ◽  
Carbonic Anhydrase Inhibition ◽  
Normal Metabolism ◽  
Acid Base Status ◽  
Erythrocyte Carbonic Anhydrase ◽  
Co2 Elimination

We studied the roles of gill and erythrocyte carbonic anhydrase in normal CO2 transfer (metabolic CO2 elimination) and in HCO3- excretion during metabolic alkalosis in the resting and swimming dogfish shark, Squalus acanthias. Gill carbonic anhydrase was selectively inhibited (greater than 98.5%) by 1 mg/kg benzolamide, which caused no physiologically significant red cell carbonic anhydrase inhibition (approximately 40%). Enzyme in both tissues was inhibited by 30 mg/kg methazolamide (greater than 99%). Both drugs caused equivalent reductions in HCO3- excretion following an infusion of 9 mmol/kg NaHCO3 as measured by the rate of fall in plasma HCO3- and by transfer into seawater. Methazolamide (red cell and gill carbonic anhydrase inhibition) caused a respiratory acidosis in fish with normal acid-base status, whereas benzolamide (gill carbonic anhydrase inhibition) did not. The only effect observed with benzolamide in these fish was a small elevation in plasma HCO3-. These findings, taken together, suggest that red cell carbonic anhydrase is required for normal metabolic CO2 elimination by the gill. Although carbonic anhydrase is located in the respiratory epithelium, it appears to have no quantitative role in transfer of metabolic CO2 to the environment, a pattern similar to all terrestrial vertebrates. However, carbonic anhydrase in the gill is crucial to this organ's function in acid-base regulation, both in the excretion of H+ or HCO3- generated in normal metabolism and in various acid-base disturbances.

PHYSIOLOGICAL RESPONSES OF THE CRAYFISH PACIFASTACUS LENIUSCULUS TO ENVIRONMENTAL HYPEROXIA: I. EXTRACELLULAR ACID-BASE AND ELECTROLYTE STATUS AND TRANSBRANCHIAL EXCHANGE

1989 ◽  
Vol 143 (1) ◽  
pp. 33-51 ◽  
Author(s):  
MICHÉLE G. WHEATLY
Keyword(s):  
Time Course ◽  
Extracellular Fluid ◽  
Respiratory Acidosis ◽  
Pacifastacus Leniusculus ◽  
Initial Increase ◽  
Flux Analysis ◽  
Freshwater Crayfish ◽  
Acid Base ◽  
Sequence Of Events ◽  
Fluid Compartment

Extracellular acid--base and ionic status, and transbranchial exchange of acidic equivalents and electrolytes, were monitored in freshwater crayfish (Pacifastacus leniusculus) during control normoxia (PO2 = 148 mmHg; 1 mmHg = 133.3 Pa), 72 h of hyperoxia (PO2 = 500 mmHg) and 24 h of recovery. An initial (3 h) respiratory acidosis of 0.2 pH units was completely compensated within 48 h by a 50% increase in metabolic [HCO3−+CO32-] accompanied by a significant reduction in circulating [Cl−]. In addition, the original increase in Pco2 was partially accommodated. The time course of transbranchial acidic equivalent exchange paralleled the change in extracellular metabolic base load with a significant branchial output of H+ during the first 48 h of hyperoxia. This was associated with net branchial effluxes of Cl− and Mg2+. Unidirectional flux analysis revealed parallel reductions in Na+ influx and efflux during initial hyperoxic exposure, reflecting an alteration in exchange diffusion. The net Cl− efflux was due to an initial increase in efflux followed by a reduction in influx. The reverse sequence of events occurred more rapidly when normoxia was reinstated: metabolic base was removed from the haemolymph and control haemolymph acid--base and ion levels were re-established within 24 h. Transbranchial fluxes of acidic equivalents similarly recovered within 24 h although net Na+ output and Cl− uptake persisted. The study attempted to identify relationships between branchial net H+ exchange and components of Na+ and Cl− exchange and quantitatively to correlate changes in the acidic equivalent and electrolyte concentrations in the extracellular fluid compartment with those in the external water.

The effects of enforced activity on ventilation, circulation and blood acid-base balance in the semi-terrestrial anuran, Bufo marinus

1980 ◽  
Vol 84 (1) ◽  
pp. 273-287
Author(s):  
D. G. McDonald ◽  
R. G. Boutilier ◽  
D. P. Toews
Keyword(s):  
Time Course ◽  
Ventilation Rate ◽  
Strenuous Exercise ◽  
Acid Base Balance ◽  
Acid Base ◽  
Arterial Blood ◽  
Base Balance ◽  
Lactate Levels ◽  
Acid Base Disturbance ◽  
Base Disturbance

Strenuous exercise results in a marked blood acid-base disturbance which is accompanied by large increases in ventilation rate, heart rate and mean arterial blood pressure. Recovery to normal resting values follows an exponential time course with a half-time of approximately 2 h for all parameters except Pa, CO2 and ventilation rate. The latter return to normal by 30 min following the exercise period. Analysis reveals that there is initially a large discrepancy between the quantity of metabolic acids buffered in the blood and the blood lactate levels. The significance of this finding is discussed. Significant changes in the concentrations of chloride, bicarbonate and lactate, in both plasma and erythrocytes, accompany the blood acid-base disturbance. Chloride and bicarbonate appear to be passively distributed between the two compartments according to a Gibbs-Donnan equilibrium whereas lactate only slowly permeates the erythrocyte.

Renal regulation of acid-base balance in the bullfrog

1961 ◽  
Vol 201 (6) ◽  
pp. 980-986 ◽  
Author(s):  
Hisato Yoshimura ◽  
Masateru Yata ◽  
Minoru Yuasa ◽  
Robert A. Wolbach
Keyword(s):  
Carbonic Anhydrase ◽  
Ammonia Excretion ◽  
Respiratory Acidosis ◽  
Acid Base Balance ◽  
Acid Base ◽  
Urinary Ph ◽  
Base Balance ◽  
Chloride Excretion ◽  
Acid Load ◽  
Renal Carbonic Anhydrase

Renal mechanisms for the maintenance of acid-base balance were studied in the normal bullfrog, during metabolic and respiratory acidosis, and after carbonic anhydrase inhibition. Following intravenous administration of 0.3–12 mmole HCl/ kg, as 0.1 n HCl, urinary pH (initially pH 6.3–7.7) did not change significantly. However, urinary ammonia excretion increased more than twofold, and within 3–5 days the cumulative increase was equivalent to the acid load given. Despite the increased ammonia excretion, chloride excretion did not increase after acid loading. In both normal and acidotic bullfrogs ammonia excretion was correlated with an increase in urinary pH. Respiratory acidosis in the small frog, Rana limnocharis, produced by exposure to 6.4% CO2 in air, induced neither urinary acidification nor increased ammonia excretion; both urinary sodium and bicarbonate excretion increased. When renal carbonic anhydrase was inhibited by acetazoleamide injection, urine flow, sodium excretion, and bicarbonate excretion increased markedly, urinary pH increased slightly, and urinary ammonia excretion remained unchanged. These renal responses to acidosis are compared with those of the acidotic dog.

CSF bicarbonate regulation in respiratory acidosis and alkalosis

1975 ◽  
Vol 38 (3) ◽  
pp. 504-511 ◽  
Author(s):  
J. Wichser ◽  
H. Kazemi
Keyword(s):  
Carbonic Anhydrase ◽  
Lactic Acidosis ◽  
Glial Cells ◽  
Respiratory Acidosis ◽  
Dissociation Curve ◽  
Cerebral Ventricles ◽  
Acid Base ◽  
Plasma Bicarbonate ◽  
Csf Lactate ◽  
The Brain

CSF bicarbonate regulation was studied in respiratory acidosis and alkalosis of 4h duration in antsthetized dogs. PCO2, pH, HCO3, ammonia, and lactate in CSF and arterial and safittal sinus bloof were measured when equal volumes of saline or acetazolamide (8 mg) were injected into lateral cerebral ventricles. The brain CO2 dissociation curve was determined at the end of all experiments. CSF and arterial bicarbonate increased 11.8 and 5.9 meg/l, respectively, in acidosis. Acetazolamide limited the rise in CSF bicarbonate to 4.2 meg/l, and prevented the CSF bicarbonate increase associated with hyperammonemia. During alkalosis CSF bicarbonate fell 6.5 meg/l and CSF lactate increased almost 2 meg/l while arterial bicarbonate fell 5.7 meg/l and lactate remained unchanged. Thus plasma bicarbonate changes account for some of the CSF unchanged. Thus plasma bicarbonate changes account for some of the CSF bicarbonate alterations in respiratory acid-base-disturbances. In acidosis additional CSF bicarbonate is formed by the choroid plexus and glial cells on the inner and outer surfaces of the brain--a reaction catalyzed by the locally present carbonic anhydrase. In alkalosis the greater fall in CSF bicarbonate than blood is due to selective brain and CSF lactic acidosis.

scholarly journals Mechanisms of acid–base regulation in seawater-acclimated green crabs (Carcinus maenas)

2016 ◽  
Vol 94 (2) ◽  
pp. 95-107 ◽  
Author(s):  
S. Fehsenfeld ◽  
D. Weihrauch
Keyword(s):  
Carbonic Anhydrase ◽  
Brackish Water ◽  
Carcinus Maenas ◽  
Ammonia Excretion ◽  
Respiratory Acidosis ◽  
Regulatory Mechanisms ◽  
Gill Epithelium ◽  
Acid Base ◽  
Bicarbonate Transporter ◽  
Bicarbonate Transporters

The present study investigated acid–base regulatory mechanisms in seawater-acclimated green crabs (Carcinus maenas (L., 1758)). In full-strength seawater, green crabs are osmoconformers so that the majority of the observed responses were attributed to ion fluxes based on acid–base compensatory responses alone. Similar to observations in brackish-water-acclimated C. maenas, seawater-acclimated green crabs exposed to hypercapnia rapidly accumulated HCO3− in their hemolymph, compensating for the respiratory acidosis caused by excess hemolymph pCO2. A full recovery from the decreased hemolymph pH after 48 h, however, was not observed. Gill perfusion experiments on anterior gill No. 5 indicated the involvement of all investigated genes (i.e., bicarbonate transporters, V-(H+)-ATPase, Na+/K+-ATPase, K+-channels, Na+/H+-exchanger, and carbonic anhydrase) in the excretion of acid–base equivalents. The most significant effects were observed when targeting a potentially cytoplasmic and (or) basolaterally localized V-(H+)-ATPase, as well as potentially basolaterally localized bicarbonate transporter (likely a Na+/HCO3−-cotransporter). In both cases, H+ accumulated in the hemolymph and CO2 excretion across the gill epithelium was significantly reduced or even reversed when blocking bicarbonate transporters. Based on the findings in this study, a working model for acid–base regulatory mechanisms and their link to ammonia excretion in the gill epithelium of C. maenas has been developed.

Relative effects of carbonic anhydrase infusion or inhibition on carbon dioxide transport and acid-base status in the sea lamprey Petromyzon marinus following exercise

1996 ◽  
Vol 199 (4) ◽  
pp. 933-940
Author(s):  
B Tufts ◽  
S Currie ◽  
J Kieffer
Keyword(s):  
Carbon Dioxide ◽  
Carbonic Anhydrase ◽  
Venous Blood ◽  
Extracellular Fluid ◽  
Respiratory Acidosis ◽  
Acid Base ◽  
Carbon Dioxide Transport ◽  
Co2 Transport ◽  
Arterial Blood ◽  
Acid Base Status

In vivo experiments were carried out to determine the relative effects of carbonic anhydrase (CA) infusion or inhibition on carbon dioxide (CO2) transport and acid-base status in the arterial and venous blood of sea lampreys recovering from exhaustive exercise. Infusion of CA into the extracellular fluid did not significantly affect CO2 transport or acid-base status in exercised lampreys. In contrast, infusion of the CA inhibitor acetazolamide resulted in a respiratory acidosis in the blood of recovering lampreys. In acetazolamide-treated lampreys, the post-exercise extracellular pH (pHe) of arterial blood was significantly lower than that in the saline-infused (control) lampreys. The calculated arterial and venous partial pressure of carbon dioxide (PCO2) and the total CO2 concentration in whole blood (CCO2wb) and red blood cells (CCO2rbc) during recovery in the acetazolamide-infused lampreys were also significantly greater than those values in the saline-infused control lampreys. These results suggest that the CO2 reactions in the extracellular compartment of lampreys may already be in equilibrium and that the access of plasma bicarbonate to CA is probably not the sole factor limiting CO2 transport in these animals. Furthermore, endogenous red blood cell CA clearly has an important role in CO2 transport in exercising lampreys.

Acid-base balance and blood and urine electrolytes of man during acclimatization to CO2

1964 ◽  
Vol 19 (1) ◽  
pp. 48-58 ◽  
Author(s):  
K. E. Schaefer ◽  
G. Nichols ◽  
C. R. Carey
Keyword(s):  
Cation Exchange ◽  
Time Course ◽  
Respiratory Acidosis ◽  
Acid Base Balance ◽  
Acid Base ◽  
Low Concentration ◽  
Base Balance ◽  
Urine Electrolytes ◽  
Two Phases ◽  
Sodium And Potassium

Acid-base balance regulation and changes in electrolyte metabolism have been studied in 20 subjects exposed to 1.5% CO2 over a period of 42 days with control periods preceding and subsequent to exposure. During exposure to CO2 a slight uncompensated respiratory acidosis was present during the first 23 days followed by a compensated respiratory acidosis. Deacclimatization was incomplete, even after 4 weeks of recovery on air. Arterial CO2 tension increased 5 mm Hg during exposure and remained at this elevated level during the first 9 days of recovery on air. In chronic respiratory acidosis the concentration of chloride in the red cells and in plasma remains practically normal, indicating that the chloride shift does not operate. Cation exchange was observed under these conditions. Sodium increased while potassium showed an approximately equivalent decrease. Sodium and potassium balance studies indicated that only sodium exhibits a pattern paralleling the two phases of acid-base balance regulation, retention being followed by increased excretion. Body weight was maintained throughout the experiment in spite of a 24–30% reduction in food intake. mild respiratory acidosis and compensation; 1.5% CO2 exposure and recovery; arterial pCO2, chloride shift, and cation exchange; sodium and potassium excretion; sodium potassium and nitrogen balance; acid-base regulation in chronic hypercapnia; time course in acid-base regulations during chronic exposure to low concentration of CO2; acclimatization and deacclimatization to low concentration of CO2 Submitted on July 22, 1963

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