368 REPORT OF THE COMMISSIONER OF FISHERIES. 



are at the bottom of the trouble. Hill and ^MacLeod (1903) have the 

 follov>ing to say: 



Paul Bert, by his remarkable experiments, published in 1878, proved that the true 

 causae 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. He also 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- arc a part of the snmmar}^ b}^ 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 the air emboli. 



Young men escape caisson sickness owing to the elasticity of their tissues and 

 greater facility for collateral pathways of circulation. 



The efferv^escence of gas in the vessels of caisson workers is of course 

 largely prevented bj' the precautions taken, but it is the logical result 

 of compression followed by rapid decompression. With fishes there 

 is, unless experimental!}', 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 W'Orker should develop the efi'ervescence 

 wdiile still under the compression, provided there is a difference of 

 temperature between the sj'stemic 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 ma}^ 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 thirt3'-six hours by an excess 

 of about 6 c. c. of nitrogen per liter. Sea spiders {Anojylodactylus)^ 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, hj'droids, and some g-reen algffi also develop and emit bubbles 

 which presumabl}^ originate in supersaturation. 



