FISHERY BULLETIN: VOL. 73, NO. 4 



sessed by using measurements of maximal swim- 

 ming performance, blood chemistry, and photic 

 response. Measurements were made on groups of 

 sur\'ivors from lethal exposure tests immediately 

 after the LEjo and LE50 points were reached or 

 following a 2-wk recovery period in 100% saturat- 

 ed water. Swimming performance was measured 

 by distance gained and time of swimming against 

 a constant water current of 1.25 m/s within a U- 

 shaped inclined trough (14 m long and 8 cm wide). 

 Blood samples were analyzed on a Techni- 

 con Sequential Multiple Analyzer (SMA 12/60).' 

 Pooled serum samples were analyzed for Ca, Na, 

 PO4 , K, CI, albumin, total protein, cholesterol, 

 alkaline phosphatase, glucose, urea, uric acid, total 

 bilirubin, lactic dehydrogenase and serum glu- 

 tamic oxaloacetic-acid transaminase. Photic re- 

 sponse was evaluated by electrophysiological 

 monitoring of the optic tectum during retina 

 stimulation with flickering light. A more detailed 

 description of the methods used in the swimming 

 performance and blood chemistry measurements 

 appear in reports by Schiewe (1974) and by New- 

 comb (1974),*^ respectively. 



RESULTS 



Relationships Among Mortality, 

 Exposure Time, and Gas Concentration 



Mean exposure times at which 10, 50, and 100% 

 mortality occurred at 120 and 125% Ng + Ar sat- 

 uration indicate no substantial difference 

 between susceptibility of juvenile chinook and 

 steelhead trout (Table 2). However, at 115% 

 N2 + Ar saturation, steelhead appeared to be more 

 susceptible than chinook; i.e., steelhead reached 

 the 50% mortality level within 35 days, whereas 

 LE5Q was never reached in test groups of chinook. 



Mortalities of control fish for all tests (105-125%) 

 ranged from to 3.3% throughout the 35-day test 

 periods. Because of the comparatively minor losses 

 of controls, data from test groups are given as 

 observed (not compensated for loss of controls). 

 Mortalities observed in tests at 105 and 110% of 

 nitrogen saturation were 5% or less for both 



species, and gas bubble disease was not the ap- 

 parent cause of death. 



The onset of mortality attributable to gas 

 supersaturation occurred at about 115% dissolved 

 nitrogen among both steelhead and chinook. 



At about 120% nitrogen saturation the means of 

 lethal exposure times to 50% mortality (LE50) 

 were 26.9 and 33.3 h for chinook and steelhead, 

 respectively. LE5q's for chinook and steelhead at 

 125% nitrogen saturation were 13.6 and 14.2 h, 

 respectively, which are similar to those (11.3 and 

 14.0 h) observed in earlier tests by Ebel et al. (1971) 

 at test concentrations of 125 to 130% N2+ Ar. Test 

 fish stocks used previously were from different 

 hatcheries and earlier brood years and were 

 slightly larger (spring chinook-23 g and 135 mm, 

 steelhead-54 g and 179 mm). 



Table 2. -Mean values of lethal exposure time for juvenile 

 steelhead and chinook acclimated to 15°C and then subjected to 

 various levels of gas saturation' from 100 to 125% in shallow 

 tanks (25-cm depth). 



^rade names referred to in this publication do not imply en- 

 dorsement of commercial products by the National Marine 

 Fisheries Service, NOAA. 



'Newcomb, T. W. 1974. Changes in juvenile steelhead (Salmo 

 gairdneri) blood chemistry foUovi^ing sublethal exposure to 

 various levels of nitrogen supersaturation. Northwest Fish. 

 Cent., Natl. Mar. Fish. Serv., NOAA, Seattle, Wash. Unpubl. 

 man user. 



'Percentage saturation of nitrogen and argon was set as Indi- 

 cated in the table {^ 2%). Oxygen concentrations ranged be- 

 tween 87 and 98% saturation in tanks set at 100-110% nitrogen 

 plus argon saturation; in tanks set a 115-125% nitrogen satura- 

 tion, Oj levels ranged between 98 and 115%. 



2Exposure times indicated for test replicates of section A only. 

 Mortality in section B had not reached indicated level at termi- 

 nation of test. 



Effect of Oxygen Concentrations on 

 Time to Death Measurements 



The role of atmospheric gases other than ni- 

 trogen (particularly oxygen) in causing gas bub- 

 ble disease has been questioned by several inves- 

 tigators. Arguments for and against the assump- 

 tion that dissolved atmospheric nitrogen is the 

 exclusive cause of gas bubble disease are prevalent 

 throughout the literature (Marsh and Gorham 

 1905; Doudoroff 1957; Egusa 1959, 1969; Shirahata 



790 



