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Chris M. Wood - One of the best experts on this subject based on the ideXlab platform.
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The effects of temperature and swimming speed on instantaneous fuel use and nitrogenous waste Excretion of the Nile tilapia.
Physiological and biochemical zoology : PBZ, 1999Co-Authors: Derek Alsop, James D. Kieffer, Chris M. WoodAbstract:Abstract The effects of acclimation temperature (30°, 20°, and 15°C) and swimming speed on the aerobic fuel use of the Nile tilapia (Oreochromis niloticus; 8–10 g, 8–9‐cm fork length) were investigated using a respirometric approach. As acclimation temperature was decreased from 30°C to 15°C, resting oxygen consumption ( \documentclass{aastex} \usepackage{amsbsy} \usepackage{amsfonts} \usepackage{amssymb} \usepackage{bm} \usepackage{mathrsfs} \usepackage{pifont} \usepackage{stmaryrd} \usepackage{textcomp} \usepackage{portland,xspace} \usepackage{amsmath,amsxtra} \usepackage[OT2,OT1]{fontenc} \newcommand\cyr{ \renewcommand\rmdefault{wncyr} \renewcommand\sfdefault{wncyss} \renewcommand\encodingdefault{OT2} \normalfont \selectfont} \DeclareTextFontCommand{\textcyr}{\cyr} \pagestyle{empty} \DeclareMathSizes{10}{9}{7}{6} \begin{document} \landscape $\mathrm{M}\,\textsc{$o$}_{2}$ \end{document} ) and Carbon Dioxide Excretion ( \documentclass{aastex} \usepackage{amsbsy} \usepackage{amsfonts} \usepackage{amssymb}...
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effects of training on respiratory gas exchange nitrogenous waste Excretion and fuel usage during aerobic swimming in juvenile rainbow trout oncorhynchus mykiss
Canadian Journal of Fisheries and Aquatic Sciences, 1997Co-Authors: Randolph F Lauff, Chris M. WoodAbstract:Fuel utilization during aerobic exercise was determined in juvenile rainbow trout that had previously undergone 2 weeks of continuous aerobic training at 25% of their maximum sustainable speed (Ucrit) and was compared with that in untrained trout. Instantaneous fuel usage was calculated from simultaneous measurements of oxygen consumption (MO ), Carbon Dioxide Excretion (MCO ), and nitrogenous waste Excretion (MN). Over 58 h of sustained aerobic exercise at 55% of Ucrit, MO and MCO remained virtually constant in the trained fish, in contrast to the significant fall over time in untrained fish, but total gas exchange was similar in the two groups. Aerobic respiratory quotient remained constant in the two treatments. MN was lower in the trained fish, resulting in a much lower (and stable) nitrogen quotient; the nitrogen quotient increased with swimming duration in the untrained fish. Lipid was the major fuel source powering aerobic exercise in both groups. Carbohydrate also played a significant role, whereas protein was of lowest quantitative importance. Training resulted in a decrease in reliance on protein and an increase in reliance on lipid metabolism. The role of protein oxidation in supporting aerobic swimming in fish, which is smaller than commonly believed, is further reduced by training.
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Adrenergic inhibition of Carbon Dioxide Excretion by trout red blood cells in vitro is mediated by activation of Na+/H+ exchange.
The Journal of experimental biology, 1991Co-Authors: Steve F Perry, Chris M. Wood, S. Thomas, Patrick J. WalshAbstract:We have used a sensitive new technique to assess the mechanism(s) of adrenergic inhibition of rainbow trout (Oncorhynchus mykiss) red blood cell (RBC) Carbon Dioxide Excretion in vitro. The effect was only apparent using blood acidified to simulate metabolic acidosis. Red blood cell CO2 Excretion was inhibited in a dose-dependent manner by physiologically relevant concentrations of noradrenaline (10–1000 nmol l-1) or adrenaline (100–1000 nmol l-1). The beta-adrenoceptor antagonist propranolol abolished the inhibitory effect of adrenaline, whereas the alpha-adrenoceptor antagonist phentolamine was without effect. The action of noradrenaline on RBC CO2 Excretion was mimicked by the beta-adrenoceptor agonist isoproterenol, but not by the alpha-adrenoceptor agonist phenylephrine. Therefore, adrenergic inhibition of CO2 Excretion is mediated by RBC beta-adrenoceptors, presumably of the beta 1 subtype. The Na+/H+ exchange inhibitor amiloride effectively blocked adrenergic stimulation of Na+/H+ exchange (as indicated from measurements of pHe and RBC pHi) and entirely prevented the inhibition of CO2 Excretion. Noradrenaline significantly reduced the rate of CO2 Excretion even in the presence of the Cl-/HCO3- exchange inhibitor SITS. Therefore, adrenergic inhibition of CO2 Excretion is accomplished via activation of RBC Na+/H+ exchange rather than by a direct inhibition of Cl-/HCO3- exchange. The observed relationship between CO2 Excretion rates and the RBC transmembrane pH difference (pHe-pHi) and the occurrence of the inhibition only at low pHe provide further evidence of the linkage with RBC Na+/H+ exchange. We suggest that adrenergic activation of RBC Na+/H+ exchange impedes CO2 Excretion by causing a rise in intracellular HCO3- levels concurrent with a reduction of intracellular PCO2. The net result is a reduced gradient for HCO3- entry into the RBC in conjunction with a diminution of the outwardly directed PCO2 gradient. Thus, the rate of formation of CO2 from the dehydration of plasma HCO3- is reduced and, in turn, a portion of this CO2 is not excreted but recycled through the red blood cell.
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A new in vitro assay for Carbon Dioxide Excretion by trout red blood cells: effects of catecholamines.
The Journal of experimental biology, 1991Co-Authors: Chris M. Wood, Steve F PerryAbstract:A new in vitro assay was developed and critically characterized to measure the rate of CO2 Excretion by trout red blood cells (RBCs) from HCO3- in their natural plasma under normal in vivo conditions of acid-base status. The assay is based on the addition of [14C]biCarbonate to the whole blood and collection of the resultant 14CO2 in the overlying gas phase. The assay simulates the exposure of blood passing through the gills, and measured CO2 Excretion rates are representative of those occurring in vivo. Rates are linear over the 3 min time course of the assay, related to haematocrit in a non-linear fashion, elevated by the addition of Carbonic anhydrase, reduced by blockade with acetazolamide, and sensitive to variations of equilibration PCO2. Large variations in plasma [HCO3-] have only a small effect on CO2 Excretion rates when the blood is chronically equilibrated at these levels. Acute elevations in [HCO3-], however, create a non-equilibrium situation, resulting in large increases in CO2 Excretion. When the blood is acidified, to duplicate typical post-exercise metabolic acidosis, adrenaline causes a marked inhibition of RBC CO2 Excretion. The response is transient, reaching a peak 5-8 min after addition of adrenaline and disappearing by 30-60 min. The magnitude of the adrenergic inhibition is correlated with the magnitude of the RBC pHi regulatory response, expressed as the RBC transmembrane pH difference (pHe-pHi). These results support the 'CO2 retention theory' explaining observed increases in blood PCO2 in vivo after exhaustive exercise and catecholamine infusions in fish.
Steve F Perry - One of the best experts on this subject based on the ideXlab platform.
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7 - Carbon Dioxide Transport and Excretion
Fish Physiology, 1998Co-Authors: Bruce Tufts, Steve F PerryAbstract:This chapter describes the process of Carbon Dioxide transport and Excretion in fishes. Metabolism produces CO 2 at variable rates that are dictated by aerobic metabolic requirements. In most fish species that have been examined, the majority of CO 2 is excreted across the gill into the water as O 2 is absorbed across the gill into the blood. The processes of O 2 uptake and CO 2 Excretion share common pathways, are governed by several mutual principles, and are intricately related. In teleost fish, the high CO 2 capacitance of true plasma predominantly reflects the buffering power of red blood cells. CO 2 added to the blood diffuses into RBCs, where extensive formation of HCO 3 - is facilitated by end-product removal. It is found that as blood arrives at the gill, it contains Carbon Dioxide predominantly in the form of HCO 3 - dissolved in the plasma. Within the transit time through the gill vasculature, sufficient HCO 3 - is converted to molecular CO 2 and excreted at a rate that matches production at the tissues. It is observed that the direct Excretion of HCO 3 - through the mechanism, though important for ionic and acid-base regulation, likely accounts for less than 5% of total Carbon Dioxide Excretion.
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Adrenergic inhibition of Carbon Dioxide Excretion by trout red blood cells in vitro is mediated by activation of Na+/H+ exchange.
The Journal of experimental biology, 1991Co-Authors: Steve F Perry, Chris M. Wood, S. Thomas, Patrick J. WalshAbstract:We have used a sensitive new technique to assess the mechanism(s) of adrenergic inhibition of rainbow trout (Oncorhynchus mykiss) red blood cell (RBC) Carbon Dioxide Excretion in vitro. The effect was only apparent using blood acidified to simulate metabolic acidosis. Red blood cell CO2 Excretion was inhibited in a dose-dependent manner by physiologically relevant concentrations of noradrenaline (10–1000 nmol l-1) or adrenaline (100–1000 nmol l-1). The beta-adrenoceptor antagonist propranolol abolished the inhibitory effect of adrenaline, whereas the alpha-adrenoceptor antagonist phentolamine was without effect. The action of noradrenaline on RBC CO2 Excretion was mimicked by the beta-adrenoceptor agonist isoproterenol, but not by the alpha-adrenoceptor agonist phenylephrine. Therefore, adrenergic inhibition of CO2 Excretion is mediated by RBC beta-adrenoceptors, presumably of the beta 1 subtype. The Na+/H+ exchange inhibitor amiloride effectively blocked adrenergic stimulation of Na+/H+ exchange (as indicated from measurements of pHe and RBC pHi) and entirely prevented the inhibition of CO2 Excretion. Noradrenaline significantly reduced the rate of CO2 Excretion even in the presence of the Cl-/HCO3- exchange inhibitor SITS. Therefore, adrenergic inhibition of CO2 Excretion is accomplished via activation of RBC Na+/H+ exchange rather than by a direct inhibition of Cl-/HCO3- exchange. The observed relationship between CO2 Excretion rates and the RBC transmembrane pH difference (pHe-pHi) and the occurrence of the inhibition only at low pHe provide further evidence of the linkage with RBC Na+/H+ exchange. We suggest that adrenergic activation of RBC Na+/H+ exchange impedes CO2 Excretion by causing a rise in intracellular HCO3- levels concurrent with a reduction of intracellular PCO2. The net result is a reduced gradient for HCO3- entry into the RBC in conjunction with a diminution of the outwardly directed PCO2 gradient. Thus, the rate of formation of CO2 from the dehydration of plasma HCO3- is reduced and, in turn, a portion of this CO2 is not excreted but recycled through the red blood cell.
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A new in vitro assay for Carbon Dioxide Excretion by trout red blood cells: effects of catecholamines.
The Journal of experimental biology, 1991Co-Authors: Chris M. Wood, Steve F PerryAbstract:A new in vitro assay was developed and critically characterized to measure the rate of CO2 Excretion by trout red blood cells (RBCs) from HCO3- in their natural plasma under normal in vivo conditions of acid-base status. The assay is based on the addition of [14C]biCarbonate to the whole blood and collection of the resultant 14CO2 in the overlying gas phase. The assay simulates the exposure of blood passing through the gills, and measured CO2 Excretion rates are representative of those occurring in vivo. Rates are linear over the 3 min time course of the assay, related to haematocrit in a non-linear fashion, elevated by the addition of Carbonic anhydrase, reduced by blockade with acetazolamide, and sensitive to variations of equilibration PCO2. Large variations in plasma [HCO3-] have only a small effect on CO2 Excretion rates when the blood is chronically equilibrated at these levels. Acute elevations in [HCO3-], however, create a non-equilibrium situation, resulting in large increases in CO2 Excretion. When the blood is acidified, to duplicate typical post-exercise metabolic acidosis, adrenaline causes a marked inhibition of RBC CO2 Excretion. The response is transient, reaching a peak 5-8 min after addition of adrenaline and disappearing by 30-60 min. The magnitude of the adrenergic inhibition is correlated with the magnitude of the RBC pHi regulatory response, expressed as the RBC transmembrane pH difference (pHe-pHi). These results support the 'CO2 retention theory' explaining observed increases in blood PCO2 in vivo after exhaustive exercise and catecholamine infusions in fish.
Patrick J. Walsh - One of the best experts on this subject based on the ideXlab platform.
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Physiological and biochemical strategies for withstanding emersion in two galaxiid fishes.
Comparative biochemistry and physiology. Part A Molecular & integrative physiology, 2014Co-Authors: Mauricio A. Urbina, Patrick J. Walsh, Jonathan V. Hill, Chris N. GloverAbstract:The galaxiid fishes of the Southern hemisphere display variable tolerance to aerial exposure. Brown mudfish (Neochanna apoda), for example, pseudoaestivate, inhabiting moist soil for months at a time, whereas inanga (Galaxias maculatus) emerse under unfavourable water conditions, but only for periods of a few hours. This study sought to identify the physiological and biochemical strategies that determine emersion tolerance in these species. Nitrogenous waste Excretion was measured before and after an experimental emersion period (14 days for mudfish, 6 h for inanga). Both species showed significantly elevated ammonia “washout” upon return to water, but no increase in plasma or muscle ammonia. Post-emersion urea levels were elevated in plasma and muscle in both fish, however the extent of the accumulation did not indicate significant de novo urea production. This was supported by the lack of carbamoyl phosphate synthetase activity in tissues. Consequently, mudfish metabolism was examined to determine whether changes in parameters such as oxygen consumption, Carbon Dioxide Excretion, and/or altered metabolic costs (represented by the key ionoregulatory enzyme Na+, K+-ATPase; NKA) could explain emersion tolerance. Oxygen consumption rates, already very low in immersed mudfish, were largely maintained over the course of emersion. Carbon Dioxide Excretion decreased during emersion, and a small, but significant, decrease in NKA was noted. These data suggest that the extended emersion capacity of mudfish may result from a generally low metabolic rate that is maintained throughout aerial exposure via cutaneous gas exchange, and which limits the production of potentially toxic nitrogenous waste.
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Adrenergic inhibition of Carbon Dioxide Excretion by trout red blood cells in vitro is mediated by activation of Na+/H+ exchange.
The Journal of experimental biology, 1991Co-Authors: Steve F Perry, Chris M. Wood, S. Thomas, Patrick J. WalshAbstract:We have used a sensitive new technique to assess the mechanism(s) of adrenergic inhibition of rainbow trout (Oncorhynchus mykiss) red blood cell (RBC) Carbon Dioxide Excretion in vitro. The effect was only apparent using blood acidified to simulate metabolic acidosis. Red blood cell CO2 Excretion was inhibited in a dose-dependent manner by physiologically relevant concentrations of noradrenaline (10–1000 nmol l-1) or adrenaline (100–1000 nmol l-1). The beta-adrenoceptor antagonist propranolol abolished the inhibitory effect of adrenaline, whereas the alpha-adrenoceptor antagonist phentolamine was without effect. The action of noradrenaline on RBC CO2 Excretion was mimicked by the beta-adrenoceptor agonist isoproterenol, but not by the alpha-adrenoceptor agonist phenylephrine. Therefore, adrenergic inhibition of CO2 Excretion is mediated by RBC beta-adrenoceptors, presumably of the beta 1 subtype. The Na+/H+ exchange inhibitor amiloride effectively blocked adrenergic stimulation of Na+/H+ exchange (as indicated from measurements of pHe and RBC pHi) and entirely prevented the inhibition of CO2 Excretion. Noradrenaline significantly reduced the rate of CO2 Excretion even in the presence of the Cl-/HCO3- exchange inhibitor SITS. Therefore, adrenergic inhibition of CO2 Excretion is accomplished via activation of RBC Na+/H+ exchange rather than by a direct inhibition of Cl-/HCO3- exchange. The observed relationship between CO2 Excretion rates and the RBC transmembrane pH difference (pHe-pHi) and the occurrence of the inhibition only at low pHe provide further evidence of the linkage with RBC Na+/H+ exchange. We suggest that adrenergic activation of RBC Na+/H+ exchange impedes CO2 Excretion by causing a rise in intracellular HCO3- levels concurrent with a reduction of intracellular PCO2. The net result is a reduced gradient for HCO3- entry into the RBC in conjunction with a diminution of the outwardly directed PCO2 gradient. Thus, the rate of formation of CO2 from the dehydration of plasma HCO3- is reduced and, in turn, a portion of this CO2 is not excreted but recycled through the red blood cell.
S. F. Perry - One of the best experts on this subject based on the ideXlab platform.
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Does gill boundary layer Carbonic anhydrase contribute to Carbon Dioxide Excretion: a comparison between dogfish (Squalus acanthias) and rainbow trout (Oncorhynchus mykiss).
The Journal of experimental biology, 1999Co-Authors: S. F. Perry, K M Gilmour, N J Bernier, C M WoodAbstract:In vivo experiments were conducted on spiny dogfish (Squalus acanthias) and rainbow trout (Oncorhynchus mykiss) in sea water to determine the potential role of externally oriented or gill boundary layer Carbonic anhydrase in Carbon Dioxide Excretion. This was accomplished by assessing pH changes in expired water using a stopped-flow apparatus. In dogfish, expired water was in acid-base disequilibrium as indicated by a pronounced acidification (delta pH=-0.11+/-0.01; N=22; mean +/- s.e.m.) during the period of stopped flow; inspired water, however, was in acid-base equilibrium (delta pH=-0.002+/-0.01; N=22). The acid-base disequilibrium in expired water was abolished (delta pH=-0.005+/-0.01; N=6) by the addition of bovine Carbonic anhydrase (5 mg l-1) to the external medium. Addition of the Carbonic anhydrase inhibitor acetazolamide (1 mmol l-1) to the water significantly reduced the magnitude of the pH disequilibrium (from -0.133+/-0.03 to -0.063+/-0.02; N=4). However, after correcting for the increased buffering capacity of the water caused by acetazolamide, the acid-base disequilibrium during stopped flow was unaffected by this treatment (control delta [H+]=99.8+/-22.8 micromol l-1; acetazolamide delta [H+]=81.3+/-21.5 micromol l-1). In rainbow trout, expired water displayed an acid-base disequilibrium (delta pH=0.09+/-0.01; N=6) that also was abolished by the application of external Carbonic anhydrase (delta pH=0.02+/-0.01). The origin of the expired water acid-base disequilibrium was investigated further in dogfish. Intravascular injection of acetazolamide (40 mg kg-1) to inhibit internal Carbonic anhydrase activity non-specifically and thus CO2 Excretion significantly diminished the extent of the expired water disequilibrium pH after 30 min (from -0.123+/-0.01 to -0.065+/-0.01; N=6). Selective inhibition of extracellular Carbonic anhydrase activity using a low intravascular dose (1.3 mg kg-1) of the inhibitor benzolamide caused a significant reduction in the acid-base disequilibrium after 5 min (from -0.11+/-0.01 to -0.07+/-0. 01; N=14). These results demonstrate that the expired water acid-base disequilibrium originates, at least in part, from excretory CO2 and that extracellular Carbonic anhydrase in dogfish may have a significant role in Carbon Dioxide Excretion. However, externally oriented Carbonic anhydrase (if present in dogfish) plays no role in catalysing the hydration of the excretory CO2 in water flowing over the gills and thus is unlikely to facilitate CO2 Excretion.
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AN EVALUATION OF FACTORS LIMITING Carbon Dioxide Excretion BY TROUT RED BLOOD CELLS IN VITRO
The Journal of Experimental Biology, 1993Co-Authors: S. F. Perry, K. GilmourAbstract:An evaluation of several potential factors limiting Carbon Dioxide Excretion by rainbow trout (Oncorhynchus mykiss) red blood cells was performed in vitro using a recently developed radioisotopic assay. Red blood cell (RBC) CO2 Excretion was reduced by pre-treatment (30 min) of blood with the Carbonic anhydrase inhibitor acetazolamide (final nominal concentration 10–4 mol l-1) or the Cl-/HCO3- exchange inhibitor SITS (4-acetamido-4′-isothiocyanatostilbene-2,2′-disulphonic acid; 10-4 mol l-1). The addition of bovine Carbonic anhydrase to plasma stimulated CO2 Excretion in a dose-dependent manner, with maximal levels of CO2 Excretion achieved at a concentration of 3 mg ml-1. These results confirmed that Carbonic anhydrase activity and/or Cl-/HCO3- exchange velocity are potential limiting factors in CO2 Excretion. Increasing the haematocrit elevated the rate of RBC CO2 Excretion, although the effect was apparent only between 0 and 15 % haematocrit; the rate of CO2 Excretion was unaffected by further increases in haematocrit between 15 and 35 %. Acute elevation of plasma HCO3- levels increased the rate of CO2 Excretion in blood but not in plasma (with or without added Carbonic anhydrase). These data suggest that HCO3- availability may limit CO2 Excretion at higher haematocrits when the Cl-/HCO3- exchange sites are most plentiful. Lysis of RBCs and the accompanying release of intracellular Carbonic anhydrase into the plasma significantly increased CO2 Excretion at all haematocrit and HCO3- levels, indicating that the velocity of Cl-/HCO3- exchange does indeed limit trout RBC CO2 Excretion. The addition of Carbonic anhydrase (3 mg ml-1) to lysed blood caused a further increase in the rate of CO2 Excretion but only at the low haematocrit of 5 %. This result suggests that the activity of RBC Carbonic anhydrase does not normally limit CO2 Excretion except at unusually low haematocrits, such as might occur during severe anaemia. The rapid oxygenation of partially deoxygenated blood during the 3 min assay caused a marked stimulation of CO2 Excretion that was concurrent with a significant decrease of RBC intracellular pH (pHi). These data indicate that the supply of Bohr protons during the oxygenation of the blood is a key factor limiting CO2 Excretion. Oxygenation of the blood prior to performing the assay also lowered RBC pHi, although CO2 Excretion was actually reduced, indicating a possible specific effect of pHi on Cl-/HCO3- exchange activity or HCO3- dehydration. The results are discussed with reference to the control of Carbon Dioxide Excretion in fish.
K. Gilmour - One of the best experts on this subject based on the ideXlab platform.
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AN EVALUATION OF FACTORS LIMITING Carbon Dioxide Excretion BY TROUT RED BLOOD CELLS IN VITRO
The Journal of Experimental Biology, 1993Co-Authors: S. F. Perry, K. GilmourAbstract:An evaluation of several potential factors limiting Carbon Dioxide Excretion by rainbow trout (Oncorhynchus mykiss) red blood cells was performed in vitro using a recently developed radioisotopic assay. Red blood cell (RBC) CO2 Excretion was reduced by pre-treatment (30 min) of blood with the Carbonic anhydrase inhibitor acetazolamide (final nominal concentration 10–4 mol l-1) or the Cl-/HCO3- exchange inhibitor SITS (4-acetamido-4′-isothiocyanatostilbene-2,2′-disulphonic acid; 10-4 mol l-1). The addition of bovine Carbonic anhydrase to plasma stimulated CO2 Excretion in a dose-dependent manner, with maximal levels of CO2 Excretion achieved at a concentration of 3 mg ml-1. These results confirmed that Carbonic anhydrase activity and/or Cl-/HCO3- exchange velocity are potential limiting factors in CO2 Excretion. Increasing the haematocrit elevated the rate of RBC CO2 Excretion, although the effect was apparent only between 0 and 15 % haematocrit; the rate of CO2 Excretion was unaffected by further increases in haematocrit between 15 and 35 %. Acute elevation of plasma HCO3- levels increased the rate of CO2 Excretion in blood but not in plasma (with or without added Carbonic anhydrase). These data suggest that HCO3- availability may limit CO2 Excretion at higher haematocrits when the Cl-/HCO3- exchange sites are most plentiful. Lysis of RBCs and the accompanying release of intracellular Carbonic anhydrase into the plasma significantly increased CO2 Excretion at all haematocrit and HCO3- levels, indicating that the velocity of Cl-/HCO3- exchange does indeed limit trout RBC CO2 Excretion. The addition of Carbonic anhydrase (3 mg ml-1) to lysed blood caused a further increase in the rate of CO2 Excretion but only at the low haematocrit of 5 %. This result suggests that the activity of RBC Carbonic anhydrase does not normally limit CO2 Excretion except at unusually low haematocrits, such as might occur during severe anaemia. The rapid oxygenation of partially deoxygenated blood during the 3 min assay caused a marked stimulation of CO2 Excretion that was concurrent with a significant decrease of RBC intracellular pH (pHi). These data indicate that the supply of Bohr protons during the oxygenation of the blood is a key factor limiting CO2 Excretion. Oxygenation of the blood prior to performing the assay also lowered RBC pHi, although CO2 Excretion was actually reduced, indicating a possible specific effect of pHi on Cl-/HCO3- exchange activity or HCO3- dehydration. The results are discussed with reference to the control of Carbon Dioxide Excretion in fish.