PRE- AND POSTBRANCHIAL CARBON DIOXIDE CONTENT OF RAINBOW TROUT (ONCORHYNCHUS MYKISS) BLOOD AFTER CATECHOLAMINE INJECTION

1993 ◽  
Vol 180 (1) ◽  
pp. 315-322
Author(s):  
M. Nikinmaa ◽  
L. Vihersaari

It is generally accepted that plasma bicarbonate is the major source of carbon dioxide excreted in the gills of teleost fish (Perry, 1986). Although anion exchange across the membrane of rainbow trout erythrocytes is rapid, with a half-time of 0.8 s for chloride equilibration at 15 °C (Romano and Passow, 1984), the rate of bicarbonate influx into the erythrocytes limits the rate of conversion of plasma bicarbonate to carbon dioxide and, thereby, carbon dioxide excretion per unit volume of blood in gills, because the residence time of blood in the secondary lamellae of the gills is only 1–6 s (Hughes et al. 1981; Bhargava et al. 1992). Thus, factors that reduce the net rate of bicarbonate influx through the anion exchanger may reduce the efficiency of carbon dioxide excretion in gills. The effect is, however, temporary. If carbon dioxide production remains constant, the reduction of carbon dioxide excretion will increase the venous carbon dioxide tension and content, thus increasing the diffusion gradient across the gills and speeding up CO2 removal until the CO2 excretion again matches production.

1978 ◽  
Vol 72 (1) ◽  
pp. 17-24
Author(s):  
M. S. Haswell ◽  
D. J. Randall

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.


1999 ◽  
Vol 202 (6) ◽  
pp. 749-756 ◽  
Author(s):  
S.F. Perry ◽  
K.M. Gilmour ◽  
N.J. Bernier ◽  
C.M. Wood

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.


1994 ◽  
Vol 192 (1) ◽  
pp. 269-284 ◽  
Author(s):  
K Gilmour ◽  
S Perry

An extracorporeal circulation in combination with a stop­flow technique was used to characterize the acid­base disequilibrium in the arterial blood of rainbow trout Oncorhynchus mykiss during environmental hypoxia, hyperoxia or hypercapnia. Arterial blood was routed from the coeliac artery through an external circuit in which pH (pHa), partial pressure of oxygen (PaO2) and partial pressure of carbon dioxide (PaCO2) were monitored continuously. The stop­flow condition was imposed by turning off the pump which drove the external loop. Water PO2 or PCO2 was adjusted to give the experimental conditions by bubbling N2, O2 or CO2 through a water equilibration column supplying the fish. During normoxia, the arterial blood exhibited a positive acid­base disequilibrium of approximately 0.04 pH units; that is, pH increased over the stop­flow period by 0.04 units. The extent of the imbalance was increased significantly by hypoxia (final PaO2=2.7­3.7 kPa; deltapH=0.05 units). In fish exposed to hyperoxia (final PaO2=47­67 kPa), the direction of the disequilibrium was reversed; pHa declined by 0.03 units. During hyperoxia, CO2 excretion was impaired by 63 % and the PCO2 of postbranchial blood was higher than that of prebranchial blood. It is therefore conceivable that a reversal of the normal, outwardly directed, diffusion gradient for CO2 accounted for the negative disequilibrium; CO2 uptake at the gills would drive plasma CO2/HCO3-/H+ reactions towards CO2 hydration and H+ formation. During hypercapnia, fish exhibited a twofold increase in the positive pH disequilibrium (deltapH=0.06 units). The results of this study confirmed the existence of an acid­base disequilibrium in the arterial blood of rainbow trout and clearly demonstrated that the extent and/or direction of the disequilibrium are influenced by the respiratory status of the fish.


1993 ◽  
Vol 50 (5) ◽  
pp. 988-995 ◽  
Author(s):  
Nils Petter Berg Justesen ◽  
Torbjørn Dall-Larsen ◽  
Leiv Klungsøyr

Particulate preparations from freshwater rainbow trout (Oncorhynchus mykiss) gill homogenates contain an active magnesium ion activated ATPase that transports protons into the vesicles. Oligomycin at a concentration of 20 μg∙mL−1 had little effect on the proton transport, which was completely inhibited by N-ethylmaleimide. This inhibition was partly counteracted by dithiothreitol. Proton transport in freshwater trout gill submitochondrial particles was completely inhibited by oligomycin. When freshwater trout were kept for 40 min in water equilibrated with air containing 5% carbon dioxide, their gill lamellar epithelium contained many cells densely covered with erect microvilli. After changing to water bubbled with room air, the cells rapidly lost their microvilli. Control fish that were killed immediately after removal from the storage tank also had microvilli, but less erect and fewer in number. Labelled latex microspheres and dextran were used as markers for external medium uptake into gill epithelial cells. The fish were pretreated by bubbling the water by air containing 5% carbon dioxide, and the uptake took place when the water was bubbled with room air.


1992 ◽  
Vol 169 (1) ◽  
pp. 235-249 ◽  
Author(s):  
Y. TANG ◽  
H. LIN ◽  
D. J. RANDALL

The carbon dioxide content of the intracellular compartment of fish muscle was determined by direct measurements of CO2 and pH in tissue homogenates of rainbow trout, Oncorhynchus mykiss. The results agree with the concept that compartmental distribution of CO2 is pH-dependent and that muscle membranes are not very permeable to bicarbonate. The interaction between CO2 and ammonia excreted from fish muscle was also investigated by altering plasma CO2 content using bicarbonate infusion following exhaustive exercise. Removal of the acid boundary layer in white muscle by bicarbonate infusion resulted in retention of ammonia in the muscle, indicating that ammonia excretion across the muscle membrane might be enhanced by the hydration of excreted CO2 in the extracellular fluid. Passive diffusion of NH3, rather than NH4+ transfer, is probably the dominant pathway of ammonia excretion through fish muscle membranes. Note: To whom reprint requests should be sent.


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