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Journal of Experimental Biology, Vol 197, Issue 1 47-63, Copyright © 1994 by Company of Biologists

JOURNAL ARTICLES

THE EFFECTS OF BRANCHIAL CHLORIDE CELL PROLIFERATION ON RESPIRATORY FUNCTION IN THE RAINBOW TROUT ONCORHYNCHUS MYKISS

S Bindon, K Gilmour, J Fenwick and S Perry

The objectives of this study were to induce chloride cell (CC) proliferation on the gill lamellae of rainbow trout Oncorhynchus mykiss and to evaluate the consequences for respiratory function. Chronic elevation of hormone levels was used to induce CC proliferation; fish were injected with a combination of cortisol (8 mg kg-1 intramuscularly every day for 10 days) and ovine growth hormone (2 mg kg-1 intraperitoneally every second day for 10 days). The extent of CC proliferation was quantified using scanning electron microscopy and a two-dimensional analysis. An extracorporeal preparation in combination with environmental hypoxia was used to assess the effects of CC proliferation on respiratory function. 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. Environmental hypoxia was imposed by gassing a water equilibration column supplying the experimental chamber with N2. The hormone treatment increased the average CC surface area by 2.7-fold and CC density by 2.2-fold; the combined effect was a fivefold increase in CC fractional area. While the PaO2 values of hormone-treated and control fish were similar at PwO2>12.0 kPa, the arterial O2 tensions of treated fish were significantly lower than those of the control group for PwO2¾12.0 kPa. In comparison with control fish at all environmental O2 tensions, the hormone-treated fish exhibited elevated PaCO2 values and a significant acidosis. The effects of CC proliferation on blood gas variables in hormone-treated fish were accompanied by a significantly elevated ventilation amplitude and a lowered ventilation frequency. The results of this study demonstrated (i) that impairment of respiratory gas transfer coincides with CC proliferation, (ii) that O2 and CO2 transfer are influenced differently and (iii) that partial compensation is achieved through physiological adjustments.

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