Specimens of Conger conger (L.) were exposed to environmental hypercapnia in a closed recirculating seawater system. Arterial plasma pH, PCO2 and bicarbonate concentration, as well as the net transfer of bicarbonate and ammonia between fish and ambient seawater, were monitored for 30 h of hypercapnia. The initial hypercapnia-induced reduction of arterial pH by about 0.4 pH units was restored to near control values within 10 h of hypercapnia by compensatory elevation of plasma bicarbonate concentration. The continuous rise in extracellular bicarbonate from about 5 to 22 mM during this time was the result of two different mechanisms. Initially, there was a net bicarbonate transfer from the intracellular space to the extracellular compartment until the net uptake of bicarbonate from the seawater started. The amount of bicarbonate originally transferred to the extracellular space was then returned to the intracellular compartment and finally the changes in both extracellular and intracellular pH were compensated by bicarbonate taken up from the environmental seawater. Since the ammonia excretion was not increased during hypercapnia and the pattern of plasma electrolyte concentrations does not favour the H+/Na+ ion exchange mechanism, it is concluded that the additional bicarbonate is gained by active HCO3-/Cl- ion exchange against the electrochemical gradient between fish and seawater.

Specimens of the larger spotted dogfish (Scyliorhinus stellaris) were electrically stimulated to exhaustion in a closed seawater recirculation system. The production of large quantities of lactic acid by anaerobic metabolism and the resultant efflux of the dissociation products, H+ and lactate, from the white musculature resulted in severe acid-base disturbances and in increases in plasma lactate concentration, the two effects having extremely different time courses. Plasma pH and bicarbonate were maximally depressed 15–30 min after exercise, whereas peak lactate concentrations of up to 30 mM were not attained before 4–8 h after exercise. The acid-base status were restored to normal 10–14 h after exercise, long before the aerobic processing of surplus lactic acid was complete 22–30 h after exercise. This behaviour can be explained on the basis of an interaction of transfer rates, buffer values and equilibria between intracellular and extracellular compartments with the transient net transfer of surplus H+ ions to the environmental water. About half of the original quantity of H+ was transferred net to the environment via the branchial epithelium during the first 8–10 h, and it was later taken up again at the rate of aerobic lactic acid processing in the metabolism of the fish, whereas a transfer of lactate was not observed at any time during the experiment. As a result, the distribution patterns of H+ and lactate differed from each other and varied with time elapsed after anaerobic exercise, leading to the apparent ‘H+ ion deficit’ which has been observed in the blood of several fish species during lactacidosis. Net transfer of H+ ions to the environment facilitates rapid normalization of the acid-base status long before the original stress, lactic acid, is removed from the organism and thus represents an effective regulatory mechanism for the defence of the internal milieu in fish.

Specimens of Larger Spotted Dogfish ( Scyliorhinus stellaris ) were acclimated to a range of temperatures for 22–28 days. The relationships of pH to acclimation temperature in the extracellular space and in three intracellular compartments were essentially the same as previously observed in 24 h acclimated dogfish (Heisler, Weitz & Weitz, 1976). In dogfish subjected to elevated inspired P CO 2 during acclimation to low temperature, there was an inversion in the relationship of acclimation temperature to plasma P CO 2 , and in that to plasma bicarbonate, whereas the relationships to pH values were unchanged. It is concluded that the temperature adaptation of the acid-base parameters is complete after 24 h of temperature acclimation. At least the following mechanisms are involved in the adjustment of pH with changes of temperature: changes of P CO 2 , changes of buffer pK values, and transmembrane transfer of bicarbonate. Apparently only one of them, the transmembrane transfer of bicarbonate, can be modulated in a sufficient range and is responsible for the final pH adjustment.

Simultaneous measurements of water velocity in the buccal chamber, and buccal and opercular hydrostatic pressure of carp have revealed surprisingly high water velocities. The high flow velocities mean that, at times, the kinetic energy of flow makes a substantial contribution to the total fluid energy. This suggests that there may be unequal distribution of hydrostatic pressures within the buccal chamber. Anatomical examinations showed that fluid channels in the buccal chamber and gill raker sieve are complex and can be expected to vary spatially and temporally throughout the respiratory cycle. It appears that there is a potential for error in many of the previous analyses of ‘gill resistance and energetics of fish breathing based solely on hydrostatic pressure measurements and the simplifying assumption of steady-state conditions.

1. Larval trout undergo a transition from cutaneous respiration to gill respiration which at 10°C is well advanced by the 18th day after hatching. 2. Resting heart rate of newly hatched trout increases during the first few days, stabilizes for a while, and then drops between the 9th and 18th day after hatching. This drop may be the result of establishment of ‘vagal tone’. 3. The basic breathing response of larval trout when hypoxic is an increase in fin movements and an increase in rate and amplitude of breathing, but breathing movements slow and weaken if environmental P O2 falls much below 40 mmHg. 4. With trout up to 8 days after hatching hypoxia causes a tachycardia. At very low P O2 levels there is a drop in heart rate and in the amount of blood pumped by the heart. Upon restoring oxygen to very hypoxic larvae, the heart rate recovers slowly, unlike the quick abolition of bradycardia of adult fish. It appears that up to the age of 8 days from hatching, trout do not have a functional bradycardia reflex associated with hypoxia. 5. The responses of larval trout to CO and to hypoxia, and of adult trout to CO, are similar in nature. It is proposed that the basic response to anoxaemia is an increase in breathing and circulation and that the adult bradycardia response to hypoxia is a superimposed mechanism which relates circulation to the quantity of oxygen presented to the gills.

1. The rate of oxygen uptake by rainbow trout does not alter during progressive deoxygenation of the environment. Blood lactate, however, shows a significant increase, indicating an increase in anaerobic metabolism during hypoxia. 2. The percentage utilization of oxygen from the water decreased from 55% to approximately 20% during hypoxia and was associated with a 13-fold increase in ventilation volume. 3. The arterial blood of a trout resting in aerated water was 95-100% saturated: the P o 2 was 122 mm. Hg and the P co 2 was 1-1.5 mm. Hg. 4. The venous blood of a resting trout was 70% saturated, had a P o 2 of 35 mm. Hg and a P co 2 , of 2.5 mm. Hg. 5. During hypoxia the percentage saturation of the arterial blood decreased to 37% and that of the venous blood to 3%. The P o 2 in the arterial blood was 10 mm. Hg; in the venous blood, 6 mm. Hg. The P co 2 in the arterial blood was 3.5-4 mm. Hg; in the venous blood, 4.5-5.00 mm. Hg respectively. 6. The ability of the fish to withstand hypoxia was related to the oxygen capacity of the blood, which was on average 9 vol.%. The red blood cells swelled during hypoxia, the hematocrit increased, but the red cell count did not alter. 7. Blood pH was 7.7, falling to 7.4 during hypoxia. 8. Cardiac output did not change during progressive hypoxia in the water, stroke volume increased to offset the decrease in heart rate.

1. Methods for cannulating the ventral aorta of the trout, which permit the measurement of blood pressure in the unanaesthetized, unrestrained, intact fish are described. 2. Rate and amplitude of breathing and blood pressure in the dorsal and ventral aortae increase during hypoxia. These changes are associated with a marked bradycardia. 3. There are increases in vascular resistance to blood flow in both respiratory and systemic circulations during hypoxia. 4. Post hypoxia is associated with large increases in ventral aortic and dorsal aortic pressures.

1. The effectiveness of oxygen uptake by the blood of rainbow trout ( Salmo gairdneri ) approaches 100%, whereas that for the removal of oxygen from water was only 11-30%. 2. Most of the carbon dioxide is removed from the blood as it passes through the gills, but the effectiveness of carbon dioxide uptake by water is very low, because of the high capacity of water for carbon dioxide compared with oxygen. 3. Moderate exercise had little effect on the effectiveness of gas exchange across the gills. The increased oxygen uptake was facilitated by an increase in the transfer factor of the gills for oxygen. There were small increases in the capacity-rate ratio of blood to water at the gills during moderate exercise. 4. Hypoxia resulted in a marked decrease in the effectiveness of oxygen uptake by the blood, but had little effect on oxygen removal from the water. Gas exchange was facilitated during hypoxia by an increase in transfer factor of the gills, but hindered by an increasing capacity-rate ratio of blood to water at the gills. 5. Gas exchange in an aquatic environment was compared with that in an aerial environment.