ABSTRACT
It has been suggested repeatedly that the mammalian response to anoxia of hyperpnoea and hypertension may be the survival in air-breathing vertebrates of a phylogenetically primitive mechanism present in fish (Marshall & Rosenfeld, 1936; Schmidt & Comroe, 1940; Schmidt, 1956; Heymans & Neil, 1958). Black (1951), reviewing the results of four previous studies on the effect of deoxygenated sea water on elasmobranch fish, concluded that there was no change in respiration, whilst Lutz (1930) showed that restriction of water flow through the dogfish pharynx (a change likely to cause anoxia) resulted in a slowing both of respiration and heart beat. Thus the evidence, fragmentary though it is, does not suggest that the response of an elasmobranch fish to anoxia is like that of a mammal. In an attempt to re-examine this problem using the common local dogfish Squalus acanthias* L., the work of Lutz has been confirmed and amplified. Reduction of the minute volume of pharyngeal flow caused bradycardia and respiratory slowing. It soon became clear, however, that the responses of the heart and of respiration were mediated by separate mechanisms. Respiratory rate was related primarily to minute volume and was much less influenced by the oxygen content of the water respired. The heart, by contrast, was reflexly slowed by anoxia, whether this was induced by a restricted flow of normally oxygenated water or an ample flow of deoxygenated water.
I am indebted to Dr J. Garrick, of the Dominion Museum, Wellington, for pointing out that Squalus lebruni Vaillant, the name previously used by me for this species, is a synonym of S. acanthias L.
