1. Damage to the gill epithelium occurs when hatched fish are killed rapidly by solutions of zinc sulphate.
2. The rate of routine oxygen uptake by lightly sedated, quiet, rainbow trout did not alter on exposure to a rapidly toxic solution of zinc sulphate. However, oxygen utilization decreased seven-fold, gill ventilation volume increased six-fold, heart rate was halved, coughing rate increased 18-fold and the Po2 of dorsal aortic blood declined.
3. Unsedated trout usually struggled on exposure to zinc. The survival time of struggling fish was reduced and oxygen uptake increased, but other physiological changes were similar to those in quiet fish.
4. The respiratory changes in poisoned trout were generally similar to changes observed earlier in the same fish under hypoxia.
5. The osmotic concentration and the concentrations of sodium, potassium, calcium, magnesium and zinc in blood were largely unaffected by immobilization in zinc sulphate solution. Trout survived a four-fold increase in zinc concentration in the blood by injection.
6. The results suggest that epithelial damage decreased the permeability of the gills to oxygen, and did not increase their permeability to cations. Zinc was not a rapid internal poison. Death was probably caused by tissue hypoxia, when maximum gill ventilation was no longer sufficient to supply the oxygen needs of the fish.