Another explanation of bubble formation 

 related to muscular activity is that an increase in 

 blood temperature as it passes from the gills to the 

 systemic circulation causes dissolved gas to come 

 out of solution (Marsh and Gorham, 1905). Increased 

 muscular activity causes a rise in body heat even in 

 poikilothermic animals. 



This experiment and others have shown that 

 fish in supersaturation experiments frequently die 

 of gas embolism shortly after disturbances such as 

 netting live fish, removing dead fish, taking super- 

 saturation measurements with the Weiss saturom- 

 eter, etc. This is probably due to the "cascading 

 bubble effect" initiated by muscular activity or 

 excitement as a response by the fish to the distur- 

 bance of the environment. 



If muscular activity or stress precipitates the 

 formation and/or release of gas nuclei from 

 peripheral vessels, it can be assumed that gas 

 emboli may be present in the blood vascular system 

 prior to the activity. Gas-filled venules were seen in 

 the fins of fish exposed to 120% and 115% levels of 

 supersaturation prior to the appearance of emboli 

 in the gills. At 110% supersaturation, similar obser- 

 vations have been made in previous experiments, 

 but were not seen in this experiment. Undoubtedly, 

 gas emboli exist in venules throughout the rest of 

 the body, but are most easily demonstrated histo- 

 logically in the fin and tail. 



Supersaturation levels causing tissue emphy- 

 sema and the development of gas emboli in 

 peripheral locations such as the fins may vary from 

 130% to 110% or below. However, the severity and 

 rate of development of such external lesions as bub- 

 bles in the fins and tail and subcutaneous emphy- 

 sema on the body surface seem to have a direct 

 relationship to time of exposure as well as the level 

 of supersaturation (i.e., lesions develop more 

 rapidly at 120% than at 115%). Fish dying of gas 

 embolism at 120% supersaturation had a greater 

 incidence of fully developed lesions than surviving 

 fish even though exposure times were approxi- 

 mately equal. This indicates that fish which were 

 more susceptible to external lesion development 

 may also be more prone to the "cascading bubble 

 effect." 



The incidence of external bubbles in steelhead 

 trout is greater in the tail than in the fins. It has 

 been reported from physical models that bubbles 

 tend to form along lines of material stress (Harvey 

 et al., 1944a). Material stress may be related to 

 swimming movement. The tail has a greater fre- 

 quency of movement than the fins when fish are in 

 moving water. Therefore, it is possible that increased 

 evidence of gas blisters in the tail is due to increased 

 movement. Similarly, the high incidence of emphy- 

 sema on the opercula may be related to mobility. 



If muscular activity is as important a factor in 

 emboli formation and release from peripheral loca- 

 tions in fish as Harvey indicates it is for mammalian 

 species, then the results of static water supersatura- 

 tion bioassays should be carefully examined and 

 compared to bioassays done in systems requiring 

 fish to swim against a current. Direct comparison 

 of supersaturation tolerances of salmonids in static 

 water versus situations where fish are forced to 

 swim have not been reported. Fig. 1 shows the 

 results of such a study in largemouth bass (Microp- 

 terus salmoides) where a significant difference in 

 tolerance to supersaturated water developed (Bouck 

 et al., 1975). Such experiments on salmonids would 

 provide data more representative of GBD in wild 

 fish and would be useful to determine permissible 

 supersaturation levels. 



Another interesting aspect of the pathogenesis 

 of GBD indicated by this data is that exposure to. 

 sublethal levels of supersaturated water may cause 

 decreased peristaltic movement of the gastro- 

 intestinal tract. Food was held in the stomach of 

 test fish (up to 54 hr at 120% and 93 hr at 115%) 

 much longer than could normally be expected. 

 In mammals, stimulation of the sympathetic ner- 

 vous system by stress factors can slow passage of 

 food in the gastrointestinal tract (Guyton, 1966). 

 High protein food may tend to "ferment" during 

 this period of delayed passage through the gut. 

 This process may permit the abnormal buildup of 

 gas, pathogenic bacteria, toxic products, heat, or 

 other causes of irritation which could damage the 

 intestinal lining. Excess dark bile-stained mucus 

 with some hyperemia of the intestinal surface 

 which was seen at necropsy in this experiment 

 indicates intestinal irritation. Such damage may 



100 



>- 80 



<* 60 

 o 



40 



20 



15° C 



'° SWIMMING 



J>' 



RESTING 



18 20 22 24 



TIME TO DEATH (HOURSI 



26 



FIC. 1 Effects of swimming activity on the mortality of large- 

 mouth bass (Micropterus salmoides) in water supersaturated to 

 140%. 



70 Stroud, Nebeker 



