368 REPORT OF THE COMMISSIONER OF FISHERIES. 
are at the bottom of the trouble. Hill and MacLeod (1903) have the 
following to say: 
Paul Bert, by his remarkable experiments, published in 1878, proved that the true 
cause of caisson sickness is the effervescence of gas in the blood and tissue juices. 
* * * He found that this gas (nitrogen) was set free on rapid decompression and 
produced embolism in the lungs, the central nervous system, etc.; and that the 
gravity of the result depended on the height of the pressure, the length of exposure, 
and the rapidity of decompression. Healso proved that the gas set free in the tissues 
might produce local swellings and emphysema. 
Bert also found that high oxygen tension acts as a general protoplasmic poison 
arresting metabolism, depressing the body temperature, and causing the discharge 
of convulsions in mammals and finally the death of all forms of life. 
The following are a part of the summary by the same authors of 
experiments of their own: 
The cause of caisson sickness is the escape of gas bubbles in the blood vessels and 
tissue fluids on decompression. An animal exposed for four hours to 8 atm. air and 
quickly decompressed is like an opened bottle of soda water. The fluids of the body 
generally effervesce. 
The varying symptoms of caisson sickness are due to the varying seat of theairemboli. 
Young men escape caisson sickness owing to the elasticity of their tissues and 
greater facility for collateral pathways of circulation. 
The effervescence of gas in the vessels of caisson workers is of course 
largely prevented by the precautions taken, but it is the logical result 
of compression followed by rapid decompression. With fishes there 
is, unless experimentally, no question of compression or decompres- 
sion, but the gas symptoms occur under the conditions of supersatu- 
ration corresponding to compression, and no lowering or removal of 
supersaturation, corresponding to decompression, is necessary. The 
reason for this lies chiefly in the temperature factor already discussed. 
Theoretically the caisson worker should develop the effervescence 
while still under the compression, provided there is a difference of 
temperature between the systemic and pulmonary circulation and the 
exposure to compression is of long duration. This exposure is actu-. 
ally limited of course to a few hours at a time, and this may explain 
the absence of serious results during compression. 
OTHER ANIMALS SUSCEPTIBLE TO GAS DISEASE. 
Fishes are not the only aquatic animals susceptible to gas disease. 
The crustacea may survive a long time with the blood in a condition 
resembling foam, and in the lobster and king crab this has been read- 
ily observed through the abdominal shell. These latter usually live 
much longer than fishes under the same conditions of excess, but a 
lobster at Woods Hole was killed within thirty-six hours by an excess 
of about 6c. c. of nitrogen per liter. Sea spiders (Anoplodactylus), as 
observed by Mr. L. J. Cole, are readily killed, the legs becoming filled 
with the gas and the color becoming much paler than in health. Mol- 
lusks, hydroids, and some green algx also develop and emit bubbles 
which presumably originate in supersaturation. 
