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The structure of the gill epithelium of adult whitefish (Coregonus lavaretus) was studied in the laboratory at pH 4.75 and pH 5.75 with and without added aluminium (Altot 150 μg 1−1). The gills of whitefish and perch (Perca fluviatilis) from acidic and circumneutral lakes were also studied. The increase in the mean arithmetic thickness of the lamellar epithelium of whitefish gills was not significant at pH 4.75 + Al, when compared with the control fish. The morphometric diffusing capacity decreased significantly, however. It was also significantly smaller in the gills of the whitefish in the acidic lake than in the circumneutral lake. Perch gills were not hypertrophic in any lake. The water pH or Al concentration had no consistent effect on the number of mucous cells in the gill epithelium of whitefish in the laboratory exposure, but mucous cells in the acidic lake whitefish were hypertrophied. No mucous cells were present in the lamellar region of the perch caught in lakes with a low Al concentration. Al was found inside the gill epithelium of whitefish both at pH 4.75 and pH 5.25 when Al (150 μg 1−1) was added to the water in the laboratory exposure. The gills of the whitefish accumulated Al in an acidic lake, also. Al was found inside the perch gill epithelium when the ambient water pH was circa 5, even when the total Al concentration of the water was low.

Summary The respiratory effects of low pH were studied in the field and laboratory. The thickness of gill epithelium was similar in perch from an acid lake to that in perch from a neutral lake. This observation suggests that gill hypertrophy was not the primary cause of death of fish in the acid lake. A 24-h acid exposure to pH 5 did not affect the blood respiratory properties and ion concentrations of rainbow trout at all. However, when the acid-exposed fish were further subjected to hypoxia, the red cell water content and chloride concentration increased, red cell ATP concentration decreased, and plasma so­ dium and chloride concentration decreased. These changes were not seen in animals maintained in neutral water and subjected to hypoxia. The loss of ions may be caused by hypoxia-induced increase in the diffusion area of the gills, and hyperventilation, which initially increases the diffusion gradient across gill epithelium.

The first gill arch ofSalmo gairdneri was fixed from normoxic (O2 saturation of the water >90%) and hypoxic (O2 saturation 25–30% for 5 days) fish at 10 °C and 18 °C, and from fish after one-day recovery from hypoxia at 18 °C. The secondary lamellae of the gills were analysed with morphometric methods for structural, haemotological and circulatory changes. During hypoxia a marked vascular distension took place at both temperatures. At both temperatures the vascular distension coincided with a shortening of the diffusion distance (36% at 10 °C and 21% at 18 °C) and a swelling of the erythrocytes (60% at 10 °C and 42% at 18 °C). The effects of these changes on the oxygen uptake of the gills are discussed.

The blood oxygen binding properties and gill secondary lamellar structure of rainbow trout acclimated to several temperatures were studied. The blood oxygen carrying capacity decreased as acclimation temperature increased from 2 to 15 °C; the decrease was probably caused by an increase in plasma volume. Also the blood oxygen affinity decreased as the acclimation temperature increased from 2 to 15 °C. This change had no effect on the oxygen loading in gills, since the efferent arterial oxygen tension was adequate for approximately 100% erythrocytic O2 saturation at all acclimation temperatures, but facilitated the oxygen unloading in tissues. At the highest acclimation temperature (18 °C) the oxygen loading in gills was facilitated by the changes in the secondary lamellar structure; the proportion of erythrocytes in the secondary lamellar capillaries was higher than at the other acclimation temperatures (2 and 10 °C).

1. Gill resistance (Rg) and oxygen transfer (To2) were measured in perfused rainbow trout gills. After perfusion the gills were analysed morphometrically. 2. Rg increased with 40% and To2 decreased with 91% during 60 min perfusion without vasoactive substances in the perfusion Ringer. 3. In presence of 10 micro M adrenaline both Rg and To2 remained stable at their starting levels throughout the experimental period (60 min). 4. With 0.2 micro M acetylcholine and 10 micro M adrenaline in Ringer Rg increased nearby to the same extent as in perfusions without vasoactive agents, while To2 was not significantly affected. 1 micro M acetylcholine increased Rg with 76% and decreased To2 with 51%. 5. The changes in Rg and To2 could be explained by structural changes in the secondary lamellae.