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Chronically catheterized rainbow trout (Oncorhynchus mykiss) were exposed to 4 mg/l (nominal concentration) of Zn2+ and their arterial oxygen tension measured. When the arterial oxygen tension had decreased to less than 50% of the original, one group of fish was sacrificed, and the structure of the gill secondary lamellae analyzed morphometrically. Two other groups of animals were allowed to recover in clean water and their arterial oxygen tension measured. After a recovery period of 24 h or 48 h the fish were sacrificed and their gills analyzed morphometrically. Associated with the decrease in arterial oxygen tension in the exposure, there was a marked increase in the arithmetic mean distance from water to blood across the gill epithelium, from 4.2 μm in control animals to 9.8 μm in exposed animals, and a consecutive decrease in the calculated morphometric diffusion capacity of the secondary lamellae. In clean water, the arterial oxygen tension fully recovered within 48 h, whereas the arithmetic mean distance from water to blood, although it decreased significantly as compared to the value at the end of the exposure, remained at an elevated level even after 48 h recovery (5.6 μm) as compared to control animals. Thus, in resting fish, diffusion limitation starts to influence the arterial oxygen tension when the arithmetic mean distance from water to blood is approximately 6 μm.

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.

The absorption rates of 4-bromophenol, 2,4-dibromophenol, 3,4,5-trichloroguaiacol, and tetrachloroveratrol across fish gill epithelium have been measured in a perfused gill preparation from rainbow trout (Oncorhynchus mykiss). In additional experiments the absorption rate of tetrachloroveratrol was measured in free swimming fish. The absorption rates were perfusion limited in gills perfused with a saline containing 2% polyvinylpyrrolidone MW 40,000 (PVP-40) as a plasma protein substitute. Replacement of PVP-40 with 2% bovine serum albumin increased the absorption rates 5-10 times, and in this case rates were not perfusion limited. Furthermore, they were not ventilation limited at ventilatory water flow rates between 0.45 and 1.5 liter/(min 100 g). Our observations suggest that the absorption rates in the presence of albumin are limited by diffusion in the epithelial cell layers. The rates measured in the perfused gills are in close agreement with those measured in vivo. We conclude that the preparation is well suited to investigate the mechanisms behind the absorption of hydrophobic compounds across fish gills and how the absorption rate is related to the physicochemical properties of the compounds, as well as to environmental factors.

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.

fish to zinc and measur~ residual oxygen concentra­ tion after sealed jar test, secondly by putting healthy fish in sealed jars with known concentration of zinc and measuring residual oxygen concentration, and canparing both the above results with residual oxygen levels of healthy fish in clean water • .Additionally we have investigated the role of gill damage in deter­ mining the residual oxygen concentration by ligating gill arches, thus lllnit~ effective gill surface area, and carrying out sealed jar tests in clean water. In order to see if tissue oxygen consump­ tion may influence the residual oxygen concentration, the tests have been carried out at different tanperatures.

Rainbow trouts (Salmo gairdneri Richardson) were exposed to sublethal concentrations of dehydroabietic acid (DHAA) (1.55 mg.1−1) or zinc (1.25 mg. I−1) in a semistatic system for 96 h. Different secondary lamellar structures were analysed morphometrically from oriented 1 μm sections. DHAA induced hypertrophy of the epithelium. The number of chloride cells was higher than in control gills. Zinc induced detachment of the epithelium from the underlying pillar cell system. The fusion of secondary lamellae reduced the surface area of the epithelium. Both substances induced a marked vasoconstriction in the secondary lamellar capillaries. The haematocrit value of the secondary lamellar blood was higher in both the exposed groups than in the control group.

Rainbow trout ( Salmo gairdneri ) fingerlings were exposed to sodium hypochlorite (NaClO) in semistatic LC 50 tests for 48 h in dechlorinated Helsinki tap water and water from Lake Vatia (21 km downstream from a kraft pulp mill). Fish were also exposed for 17 days to Lake Vatia water after which an acute exposure to sodium hypochlorite was made, for which physiological samples were analyzed. The 48 h LC 50 of bleached kraft pulp mill effluent was 35%. The 17 days' caging period in the recipient water 21 km downstream from the mill caused disturbances in osmotic regulation, depletion of liver glycogen and inhibition of liver UDP-glucuronosyltransferase. The gills of the exposed fish were microscopically examined. The epithelium of the secondary lamellae in the NaClO exposed gills was thicker than in the controls (48 h LC 50 0.35 mg Cl 2 /l) and the lamellae were curled with constricted blood spaces. The gill epithelium of fish exposed to NaClO in water from Lake Vatia was swollen and vacuolized (48 h LC 50 0.09 mg Cl 2 /l). The gills of fish exposed to 20% pulp mill effluent as well as the gills of fish acclimatized for 17 days in Lake Vatia water were quite normal in structure. However, after hypochlorite exposure the gills of the pre-acclimatized fish were almost totally destroyed (48 h LC 50 0.07 mg Cl 2 /l).

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.