FASTING CONFINEMENT EFFECTS ON SHARKS 635 



in capture. Typically, these animals become immobile; eventually gill 

 movements weaken and finally cease at death. A similar immobility and 

 decrease in respiratory activity may be elicited in active elasmobranchs by 

 lowering the oxygen content of the surrounding water (Fishman 1967; 

 Piiper, Baumgarten, and Meyer 1970; Satchell 1960), and is considered a 

 response to hypoxia. 



Black (1958) reviewed literature on death caused by hyperactivity in 

 fishes. He suggested that the likely cause of death involved an accumulation 

 of large amounts of lactic acid produced by anaerobic glycolysis during 

 exercise. In Scyliorhinus canicula, electric shock produced a fall in pH to 

 approximately 7; minimum values were reached 2 h after treatment (Piiper 

 and Baumgarten 1969). The pH values returned to normal 8 h later. Piiper, 

 Meyer, and Drees (1972) reported that peak lactic acid levels of more than 

 200 mg% were observed in Scyliorhinus canicula up to 8 h after 25 min of 

 activity. Presumably, the animals that survived this lactate load were capable 

 of buffering the hydrogen ions that accompanied it. Lactate metabolism in 

 captive Squalus is very slow (Robin, Murdaugh, and Millen 1966; Murdaugh, 

 Robin, and Drewry 1965). 



It may be significant that the livers of fasting rats (but not feeding rats) 

 show an impaired ability to metabolize lactate in the absence of gluco- 

 corticoids (Newsholme and Start 1973), considering the apparent lack of 

 glucocorticoid activity in elasmobranch interrenal secretions discussed above. 

 Squalus acanthias held in laboratory tanks have been reported to have higher 

 levels of blood lactate than those assayed either at the time of capture or in 

 dockside live cars. These lactate levels severely limited the animals' abilities 

 to tolerate further lactic acid loading (Murdaugh and Robin 1967). Thus it 

 appears that exertions like those associated with capture produce large 

 quantities of lactic acid, which remains in the circulation and may be 

 augmented with increasing time in captivity. 



Besides reducing the adaptability of the blood buffer system, elevated 

 levels of blood lactate are alleged to have other deleterious effects. 

 Reduction in the oxygen binding capacity of the blood, deformation of red 

 blood cells, and a tendency toward hemolysis were reported by von 

 Buddenbrock (1936) in cod and flatfish. Erythrocytes of carp and suckers 

 swelled and hemolyzed in the presence of lactate concentrations of 270 mg% 

 (Black and Irving, 1938); this is within the range of values previously noted 

 in stressed Scyliorhinus canicula (Piiper et al. 1972). Thus it is possible that 

 elevated lactate levels in captive Squalus resulted in erythrocyte destruction. 



It would be difficult to attribute the decline in hematocrit to a single 

 factor, however. Starvation reduces hematocrit values in rajids (Hartman et 

 al. 1941), cod (Kamra 1966), and eels (Sano 1962). Hematocrit also declines 

 under sampling stress (Wood and Randall 1970; Tamura, Yasuda, and Fujiki 

 1962) or following interrenalectomy (Biedl 1913; rajids). 



The decline in hematocrit was accompanied by hypertrophy and increased 

 pigment content of the reticuloendothelial cells of the spleen. Oddly shaped 

 red blood cells and intravascular hemolysis increased, while erythroblasts and 

 hemocytoblasts formed an increasing proportion of the circulating cells. 



