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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 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.

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.

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.