Abstract

Adult rainbow trout (Oncorhynchus mykiss) were acclimated to artifcial soft water to evaluate potential physiological responses compensating for the thickening of the blood-to-water diffusion barrier that is known to accompany branchial lamellar chloride cell proliferation. Indirect estimates of gill ventilation volumes using the Fick principle demonstrated pronounced hyperventilation in the softwater-acclimated fish (2,280 ± 434 mL min⁻¹ kg⁻¹) when compared to the control fish (1,217 ± 166 mL min⁻¹ kg⁻¹). Despite the hyperventilation, the soft-water-acclimated fish displayed significantly lowered arterial Po₂ values (93.7 ± 2.4 Torr [1 Torr = 133.32 Pa] vs. 102.5 ± 1.6 Torr); arterial Pco₂ was unaffected by acclimation to soft water. An in vitro radioisotopic assay was used to demonstrate that an intrinsic acceleration in the rate of HCO⁻₃ flux through the red blood cell and hence accelerated H₂CO₃ dehydration was not contributing to the maintenance of arterial Pco₂ in the soft-water-acclimated fish. The construction of blood O₂ equilibrium curves in vitro revealed an increased affinity of haemoglobin-O₂, binding in the soft-water-acclimated fish (P50 = 12.3 ± 1.3 Torr) when compared to the controls (17. 6 ± 0.9 Torr). In response to hypoxia (water Po₂ = 30 - 90 Torr), both groups of fish released catecholamines into the circulation. However, catecholamine release occurred at higher levels of water Po₂ (80 Torr compared to 50 Torr) in the soft-water-acclimated fish. The results demonstrate that prolonged exposure of rainbow trout to soft water promotes several physiological responses that may serve to alleviate or reduce the detrimental consequences of the thickened diffusion barrier elicited by chloride cell proliferation.

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