Buffering limits plasma HCO3- dehydration when red blood cell anion exchange is inhibited

Theory suggests that HCO3- dehydration in the plasma of rainbow trout is limited by both the absence of carbonic anhydrase (CA) activity and the low non-bicarbonate buffer capacity of the plasma (betaplasma). The potential for betaplasma to limit plasma HCO3- dehydration was assessed in rainbow trout in which HCO3- dehydration via the red blood cell (RBC) was inhibited using the anion exchange blocker 4,4'-diisothiocyanostilbene-2,2'-disulphonic acid (DIDS). DIDS administration reduced the rate of RBC HCO3- dehydration by 68-80% for at least 6h, resulting in the elevation of arterial CO2 tension (PaCO2) by 3.07 +/- 0.45 Torr (N = 6). Addition of bovine CA to the circulation of DIDS-treated trout caused PaCO2 to decrease significantly. This effect was increased significantly in rainbow trout in which betaplasma was elevated experimentally by intravascular injection of N-[2-hydroxyethyl]piperazine-N'-[2-ethanesulfonic acid] (HEPES), supporting the hypothesis that CA-catalysed HCO3- dehydration in the plasma of rainbow trout is limited by proton availability.