whales do not develop suffi- cient gas supersaturation in the tissues on ascent to cause extensive bubble formation in the liver.
neither decompression theory nor observation support the existence of a natu- rally occurring DCS in whales that is char- acterized by encapsulated, gas-filled cavities in the liver.
Not enough gas is taken up to produce bubbles
except possibly during multiple rapid dives to depths approaching that of the lung’s closing volume
Jepson et al. do not explain why DCS, if it did occur in the whales they investigated, should affect the liver dispro- portionately.
large gas-filled cavities in the liver, many encapsulated in dense fibrous tissue, are inconsistent with the pathology of DCS in humans and other mammals in which the bones, joints, lungs and central nervous system are primarily affected.
identifying the cetacean gas disease with DCS is premature because its pathology not only differs from that underlying the syndrome in other mam- mals, but it also cannot be explained by any physiological mechanism related to diving.
increasing concentrations of nitrogen in cetacean tissues after repetitive diving have been studied empirically in bottlenose dolphins (Tursiops truncatus)3 and higher levels are predicted for northern bottlenose whales (Hyperoodon ampullatus) on the basis of their rate of descent or ascent and depth of diving
As cetaceans differ from humans behav- iourally (as obligate, repetitive breath-hold divers), physiologically (for example, in their diving reflex)9 and anatomically (as in their retia mirabilia, large portal veins and diaphragmatic sphincters)10,11 , it may be too simplistic to assume that the distribution, severity and chronicity of lesions induced by gas emboli will be similar in both human divers and free-living cetaceans.