scholarly journals Short Circuiting of the Ocular Oxygen Concentrating Mechanism in the Teleost Salmo gairdneri Using Carbonic Anhydrase Inhibitors

1974 ◽  
Vol 64 (3) ◽  
pp. 263-273 ◽  
Author(s):  
Michael B. Fairbanks ◽  
J. Russell Hoffert ◽  
Paul O. Fromm

Ocular oxygen concentration by the process of counter current multiplication in rainbow trout (Salmo gairdneri) was rapidly suppressed after intraperitoneal injections of the carbonic anhydrase inhibitor CL-11,366. The rapidity with which this drug acted suggested a short circuiting of the choroidal rete mirabile. A comparison was made between the time after injection of inhibitor at which oxygen concentrating ability was lost to the time after injection of inhibitor at which its presence in red blood cells, choroidal rete, pseudobranch, and retinal tissue was first noted. A scheme for the possible role of carbonic anhydrase from each of these tissues in the process of ocular oxygen concentration is given.

1989 ◽  
Vol 256 (4) ◽  
pp. C728-C735 ◽  
Author(s):  
R. Motais ◽  
B. Fievet ◽  
F. Garcia-Romeu ◽  
S. Thomas

Erythrocytes of rainbow trout respond to adrenergic stimulation by activation of a Na+-H+ exchange. When red blood cells are suspended in their own plasma and equilibrated with a convenient gas mixture in a tonometer, the extrusion of H+ induces a fast, very strong acidification of the blood (by 0.5-0.7 pH units), explained as follows. Excretion of H+ into a medium containing HCO3- causes the formation of H2CO3. The uncatalyzed dehydration of H2CO3 is slow so that H+ accumulates above the level that would prevail at equilibrium, promoting a strong acid disequilibrium pH. Then the blood pH progressively returns to a value close to its initial value because of the slow uncatalyzed dehydration of H2CO3 and washout of the CO2 so produced. The period of acid disequilibrium pH, however, is lengthened because part of the CO2 generated by the spontaneous dehydration is not washed out by tonometry but diffuses into the red cells where it is rapidly converted into HCO3- and H+ by carbonic anhydrase and then excreted by Na+-H+ and Cl-HCO3- exchangers. This recycling process "refuels" the ionic reaction, increasing the time needed to reach equilibrium. The anion exchanger does not sense this strong acid disequilibrium pH, since the external HCO3- concentration is practically unchanged at that time. During the extracellular pH (pHe) recovery period, simultaneously extracellular HCO3- content decreases and intracellular Cl- content increases. Thus intracellular pH and pHe appear to be uncoupled. This overall interpretation is confirmed by experiments using carbonic anhydrase and drugs such as propranolol and amiloride.(ABSTRACT TRUNCATED AT 250 WORDS)


1987 ◽  
Vol 3 (2) ◽  
pp. 83-90 ◽  
Author(s):  
Thomas A. Heming ◽  
David J. Randall ◽  
Madeleine M. Mazeaud

1986 ◽  
Vol 65 (2) ◽  
pp. 223-234 ◽  
Author(s):  
Thomas A. Heming ◽  
David J. Randall ◽  
Robert G. Boutilier ◽  
George K. Iwama ◽  
Dennis Primmett

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