|
SCHRECK ET AL.: ELECTROSHOCK: PHYSIOLOGICAL RESPONSES BY TROUT 83
<br />present study glucose concentrations in the
<br />shocked trout were still exhibiting an increasing
<br />trend after 6 h. In a preliminary study in which
<br />we employ an experimental design similar to that
<br />discussed here, but in which we collected samples
<br />12, 24, and 48 h post shocking, we found that
<br />glucose levels returned to baseline levels by 12 h
<br />after shocking.
<br />The rapid increase in corticoids may be part
<br />of a general adaptation syndrome. Corticoids,
<br />along with factors treated above, may help ac-
<br />count for the change in glucose levels and leuco-
<br />cyte composition in the shocked trout. Prelim-
<br />inary indications are that these steroids decrease
<br />to preshock levels by l2 h post treatment. After
<br />an immediate increase in the relative abundance
<br />of thrombocytes, a downward trend was evident
<br />at 6 h; this trend apparently continued throughout
<br />the 48 h test. Heterophils increased in relative
<br />abundance. Consequently, caution should be exer-
<br />cised in using electrofishing for collecting speci-
<br />mens for physiological measurements from the
<br />field. Shocking would not influence results of
<br />biochemical systematic studies because no changes
<br />in isozyme patterns were noted. Relative quanti-
<br />ties of proteins may change in shocked trout, how-
<br />ever, as reported by Bouck and Ball (1966) and
<br />Thurston (1967),
<br />Our findings suggest that the trout were re-
<br />sponding to the electroshock as though they were
<br />suffering from extreme muscular exertion and/or
<br />hypoxia. The electroshocked fish were not able to
<br />respire normally and their circulatory efficiency
<br />was most likely impaired. This condition probably
<br />was initiated at the time of electrode activation
<br />and persisted for 1 min or more after the shock
<br />was discontinued, thereby creating a transient
<br />hypoxic state. Concomitantly, the total muscular
<br />tetany during shocking probably helped account
<br />for the utilization of energy and oxygen and the
<br />resultant responses to the oxygen debt. Neither
<br />calcium nor magnesium, both intimately involved
<br />in muscle contraction, were measurably affected.
<br />As Halsband (1967) noted, the variation in meta-
<br />bolic intensity after shock may be due to several
<br />factors including direct effect on the mechanism
<br />regulating respiratory activity, influence on mus-
<br />cular activity and motor movements of the cir-
<br />culatory system, and alterations in chemical com-
<br />position of cell substance and inclusions.
<br />It appears that death of fish collected by elec-
<br />trofishing may be the result of both acute and
<br />chronic factors. Immediate death is probably due
<br />to direct trauma such as failure of respiration
<br />ability, hemorrhaging, and fractured vertebrae.
<br />Death occurring hours after shocking is most
<br />likely the result of the combined effects of
<br />trauma, the factors associated with paying off the
<br />oxygen debt, and the exhaustion phase of the
<br />stress general adaption syndrome. Caution con-
<br />cerning asumptions in practices such as mark-
<br />recapture population estimates employing electro-
<br />shocking is warranted. Our data indicate that
<br />shocked fish are not fully recovered from the
<br />shocking simply because they have regained their
<br />equilibrium or even are able to swim. A substan-
<br />tial period of time is involved for the fish to
<br />return to "normal" preshock conditions. The
<br />question now in need of testing is that raised by
<br />the failure of the trout to fully recover from the
<br />shock within the span of a working day -would
<br />the assumptions of equal vulnerability be met in
<br />mark-recapture population estimations in which
<br />fish are marked, released, and recaptured on the
<br />same day?
<br />Acknowledgments
<br />We appreciate the assistance, fish, and space pro-
<br />vided by the U.S. National Fish Hatchery, Wythville,
<br />V a.
<br />BLACK, E. C., A. C. ROBERTSON, A. R. HANSLIP, AND W.
<br />CHID. 1960. Alterations in glycogen, glucose and lac-
<br />tate inrainbow and Kamloops trout, Salmo kairdnerr,
<br />following muscular activity. J. Fish Res. Board Can.
<br />17:487-500.
<br />BOCCARDY, J. A., AND E. L. COOPER. 1963. The use of
<br />rotenone and electrofishing in surveying small
<br />streams. Trans. Am. Fish. Soc. 92: 307-310.
<br />BODRUVA, N. V., AND B. V, KRAIUKHIN. I9S8. The reac-
<br />tions offish to electric current. Tr. Soveshch. Ikhtiol.
<br />Kom. Akad. Nauk SSSR 8: 124-131.
<br />BoucK, G. R., AND R. C. BALL. 1966. Influence of capture
<br />methods on blood characteristics and mortality in the
<br />rainbow trout (,Salmo gairdneri). Trans. Am. Fish.
<br />Soc. 9S : 170-176.
<br />CAILLOUF_T, C. W. JR. 1967. Hyperactivity, blood lactic
<br />acid and mortality in channel catfish. Agric. Home
<br />Econ. Exp. Stn., Iowa State Univ. Sci. Tech., Res.
<br />Bull. SS I :898-915.
<br />CHAVIN, W., AND J. E. YouNG. 1970. Factors in the de-
<br />termination of normal serum glucose levels of
<br />goldfish, Carassius aaratrrs L. Comp. Biochem.
<br />Physiol. 33: 629-653.
<br />CHESTER JONES, I., D. K. O. CHAN, I. W. HENDERSON,
<br />AND J. N. BALL. 1969. The adrenocortical steroids,
<br />adrenocroticotropinavd the corpuscles of Stannius, p.
<br />321-376. /n W. S. Hoar and D. J. Randall [ed.] Fish
<br />physiology. Vol. 2. Academic Press, Inc., New York,
<br />N.Y.
<br />CLAYTON, J. W., AND D. N. TRETIAK. 1972. Amine-Glrate
<br />buffers For pH control in starch gel electrophoresis. J.
<br />Fish. Res. Board Can. 29: 1169-1172.
<br />COCHRAN, W. G., AND G. M. Cox. 1957. Experimental
<br />designs. John Wiley and Sons, ]nc., New York, N.Y.
<br />481 p.
<br />COLLINS, G. B., C. D. VOI_z, AND P. S. TREFETHEN. 1954.
<br />Mortality of salmon fingerlings exposed to pulsating
<br />
|