Blood acid-base regulation during environmental hyperoxia in the rainbow trout (Salmo gairdneri).

Blood acid-base balance, blood gases, respiration, ventilation, and renal function were studied in the rainbow trout during and following sustained environmental hyperoxia (PIO2 = 3.50-650 Torr). Animals were chronically fitted with dorsal aortic cannulae for repetitive blood sampling, oral membranes for the measurement of ventilation, and bladder catheters for continuous urine collection. Hyperoxia caused a proportional increase in arterial O2 tension and a stable 60% reduction in ventilation volume (Vw), the latter mainly due to a decrease in ventilatory stroke volume. O2 consumption exhibited a short-term elevation. Arterial CO2 tension (PaCO2) rose within 1 h, causing an immediate drop in arterial pH (pHa), and continued to increase gradually thereafter, reaching a value 2-4x the normoxic control level after 96-192 h. Compensation of the associated acidosis by the accumulation of [HCO3-] in the blood plasma started within 5-6 h, and was complete by 48 h. Therefore, further compensation occurred simultaneously with the gradual rise in PaCO2. The kidney played an important active role in this compensation by preventing excretion of the accumulated [HCO3-]. Upon reinstitution of normoxia, PaCO2 dropped to control levels within 1 h, and restoration of blood acid-base status by reduction of [HCO3-] had commenced by this time. A complete return to control values occurred within 20 h. During hyperoxia, an experimental elevation of the depressed Vw above control normoxic levels caused only a minor and transient reduction in PaCO2 and no change in pHa, but injection of branchial vasodilator 1-isoprenaline (10 mumol/kg) produced a large drop in PaCO2 and rise in pHa. It is concluded that the rise in PaCO2 during hyperoxia is mainly due to internal diffusive and/or perfusive limitation associated with branchial vasoconstriction, rather than to external convective limitation associated with the decreased Vw.