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 Dependence of the Oxygen-Concentrating Mechanism of the Teleost Eye (Salmo gairdneri) on the Enzyme Carbonic Anhydrase

1969 ◽  
Vol 54 (2) ◽  
pp. 203-211 ◽  
Author(s):  
Michael B. Fairbanks ◽  
J. Russell Hoffert ◽  
Paul O. Fromm
Keyword(s):  
Carbonic Anhydrase ◽  
Environmental Water ◽  
Salmo Gairdneri ◽  
Complete Suppression ◽  
Oxygen Inhibition ◽  
Rete Mirabile ◽  
Arterial Blood ◽  
Concentrating Mechanism ◽  
The One ◽  
Erythrocyte Carbonic Anhydrase

Microoxygen polarographic electrodes were constructed and used to measure oxygen tension (POO2) in the eyes of rainbow trout (Salmo gairdneri). The values obtained are compared with arterial blood and environmental water POO2 and indicate that there is an oxygen-concentrating mechanism in the eye supplying oxygen to the avascular retina. Anatomically similar retes suggest that the mechanism is similar to the one which exists in the swim bladder. Elimination of the arterial blood supply to the choroidal gland rete mirabile of the eye (through pseudobranchectomy) and the consequent lowering of ocular oxygen tensions implicate the choroidal gland as one of the major components of the oxygen-concentrating mechanism. After pseudobranchectomy the presence of ocular POO2 above that of arterial blood is indicative of a secondary structure in the eye capable of concentrating oxygen. Inhibition of carbonic anhydrase, using acetazolamide, is shown to result in complete suppression of the oxygen-concentrating mechanism. A hypothesis is advanced for the participation of retinal-choroidal and erythrocyte carbonic anhydrase in the oxygen-concentrating mechanism.

Direct evaluation of acidification by rat testis and epididymis: role of carbonic anhydrase

1990 ◽  
Vol 258 (1) ◽  
pp. E143-E150 ◽  
Author(s):  
C. R. Caflisch ◽  
T. D. DuBose
Keyword(s):  
Carbonic Anhydrase ◽  
Co2 Concentration ◽  
Seminiferous Tubules ◽  
Direct Evaluation ◽  
Rat Testis ◽  
Arterial Blood ◽  
Co2 Concentrations ◽  
Primary Fluid ◽  
Cauda Epididymidis

The present experiments have employed microelectrode techniques (pH and PCO2) and microcalorimetry (total CO2 concentration) to define parameters of acidification in specific structures of the rat testis and epididymis during control conditions and after administration of the carbonic anhydrase inhibitor acetazolamide (20 or 50 mg/kg). Values for in situ pH during control conditions in seminiferous tubules (ST; 6.96 +/- 0.01), proximal caput (PCP; 6.62 +/- 0.01), middle caput (MCP; 6.59 +/- 0.01), middle corpus (MCR; 7.10 +/- 0.02), and proximal cauda epididymidis (PCD; 6.85 +/- 0.01) were significantly more acidic than in testicular artery (TA; 7.36 +/- 0.01) or systemic arterial blood (SAB; 7.40 +/- 0.01) and did not change significantly after acetazolamide. In situ partial pressure of CO2 (PCO2) in TA (52.2 +/- 0.6 mmHg), ST (52.3 +/- 0.4 mmHg), PCP (52.9 +/- 0.4 mmHg), MCP (53.0 +/- 0.7 mmHg), MCR (53.4 +/- 0.4 mmHg), and PCD (52.4 +/- 0.4 mmHg) were indistinguishable from each other, but all values were significantly higher than SAB PCO2 (39.2 +/- 0.5 mmHg). Acetazolamide increased in situ PCO2 significantly in all structures except the MCR. The total CO2 concentration in normal ST fluid (10.7 +/- 0.5 mM) was significantly higher than in "primary" fluid (6.9 +/- 0.3 mM), and both values were well below TA (26.9 +/- 1.3 mM) or SAB (24.6 +/- 0.4 mM) total CO2 concentrations. In the epididymis, total CO2 concentrations were indistinguishable and not different from the value in primary fluid.(ABSTRACT TRUNCATED AT 250 WORDS)

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.

Inhibitor sensitivity of pulmonary vascular carbonic anhydrase

1993 ◽  
Vol 75 (4) ◽  
pp. 1642-1649 ◽  
Author(s):  
T. A. Heming ◽  
C. G. Vanoye ◽  
E. K. Stabenau ◽  
E. D. Roush ◽  
C. A. Fierke ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Carbonic Anhydrase ◽  
Luminal Surface ◽  
Membrane Permeation ◽  
Vascular Activity ◽  
Capillary Endothelial Cells ◽  
Membrane Bound ◽  
Co2 Excretion ◽  
Isolated Rat

The inhibitor sensitivity of pulmonary vascular carbonic anhydrase (CA) was examined in situ to identify the specific isozyme responsible for vascular activity and to study its distribution in the lung. Vascular CA activity was monitored in isolated rat lungs by measuring the rate of CO2 excretion and the magnitude of postcapillary CO2-HCO(3-)-H+ disequilibria. Lungs were perfused with isotonic salines containing gluconate, sulfate, Cl-, or I-, with or without sulfonamide derivatives. Effects of a CA inhibitor purified from porcine blood plasma were also determined. Vascular CA activity was unaffected by gluconate, sulfate, Cl-, and I- (< or = 100 mM). Sulfonamides with vastly different rates of membrane permeation (i.e., readily permeating ethoxzolamide, slowly permeating acetazolamide, and membrane-impermeant quaternary ammonium sulfanilamide) were capable of accessing all vascular CA with similar rates of access. The porcine inhibitor of CA (340 nM) produced a significant, but submaximal, inhibition of vascular CA activity. The data suggest that pulmonary vascular activity reflects a high-activity membrane-bound isozyme, CA IV, which is located on the extracellular luminal surface of capillary endothelial cells.

In situ characterization of carbonic anhydrase activity in isolated rat lungs

1990 ◽  
Vol 69 (6) ◽  
pp. 2155-2162 ◽  
Author(s):  
T. A. Heming ◽  
A. Bidani
Keyword(s):  
Carbonic Anhydrase ◽  
Time Course ◽  
Carbonic Anhydrase Activity ◽  
In Situ Characterization ◽  
Rat Lungs ◽  
Isolated Lungs ◽  
Menten Constant ◽  
Co2 Excretion

Lung carbonic anhydrase (CA) participates directly in plasma CO2-HCO3(-)-H+ reactions. To characterize pulmonary CA activity in situ, CO2 excretion and capillary pH equilibration were examined in isolated saline-perfused rat lungs. Isolated lungs were perfused at 25, 30, and 37 degrees C with solutions containing various concentrations of HCO3- and a CA inhibitor, acetazolamide (ACTZ). Total CO2 excretion was partitioned into those fractions attributable to dissolved CO2, uncatalyzed HCO3- dehydration, and catalyzed HCO3- dehydration. Approximately 60% of the total CO2 excretion at each temperature was attributable to CA-catalyzed HCO3- dehydration. Inhibition of pulmonary CA diminished CO2 excretion and produced significant postcapillary perfusate pH disequilibria, the magnitude and time course of which were dependent on temperature and the extent of CA inhibition. The half time for pH equilibration increased from approximately 5 s at 37 degrees C to 14 s at 25 degrees C. For the HCO3- dehydration reaction, pulmonary CA in situ displayed an apparent inhibition constant for ACTZ of 0.9-2.2 microM, a Michaelis-Menten constant of 90 mM, a maximal reaction velocity of 9 mM/s, and an apparent activation energy of 3.0 kcal/mol.

IN SITU AND PILOT ORGAN PERFUSION TECHNIQUES FOR THE STUDY OF METABOLIC DYNAMICS

1972 ◽  
Vol 68 (2_Supplb) ◽  
pp. S9-S25 ◽  
Author(s):  
John Urquhart ◽  
Nancy Keller
Keyword(s):  
Cardiac Output ◽  
Large Fraction ◽  
Experimental Studies ◽  
Test Substance ◽  
Organ Perfusion ◽  
Systemic Blood ◽  
Experimental Control ◽  
Arterial Blood ◽  
Vascular Connections

ABSTRACT Two techniques for organ perfusion with blood are described which provide a basis for exploring metabolic or endocrine dynamics. The technique of in situ perfusion with autogenous arterial blood is suitable for glands or small organs which receive a small fraction of the animal's cardiac output; thus, test stimulatory or inhibitory substances can be added to the perfusing blood and undergo sufficient dilution in systemic blood after passage through the perfused organ so that recirculation does not compromise experimental control over test substance concentration in the perfusate. Experimental studies with the in situ perfused adrenal are described. The second technique, termed the pilot organ method, is suitable for organs which receive a large fraction of the cardiac output, such as the liver. Vascular connections are made between the circulation of an intact, anaesthetized large (> 30 kg) dog and the liver of a small (< 3 kg) dog. The small dog's liver (pilot liver) is excised and floated in a bath of canine ascites, and its venous effluent is continuously returned to the large dog. Test substances are infused into either the hepatic artery or portal vein of the pilot liver, but the small size of the pilot liver and its blood flow in relation to the large dog minimize recirculation effects. A number of functional parameters of the pilot liver are described.

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