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  • 1
    ISSN: 1573-1448
    Keywords: cyanide ; stress ; liver O2 consumption
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology
    Notes: Abstract The lethality, anaesthetic and physiological effects of ‘pulsed’ cyanide (CN-) exposures to a common tropical marine fish Dascyllus aruanus were assessed. Cyanide (25 and 50mgl-1) was applied as pulses (10, 60 and 120 s) to fish under non-stressed and stressed (by chasing and/or placing fish under hypoxic stress) conditions. Following treatment, the time until recovery and the percent survival were determined. The fish were allowed a 2.5 week recovery period from the treatments at which time four physiological end-points were measured: (1) the blood haemoglobin content, (2) the percent blood O2 content, (3) the liver rhodonase activity and (4) the liver O2 consumption rate. The greater the CN- concentration and exposure time, the longer the recovery time. Non-stressed fish exposed to 10 s pulses of 25 mgl-1 of CN- fully recovered within 4 min whereas fish exposed for 60 s and 50 mgl-1 of CN- required up to 50 min for full recovery. Exposure for 120 s at 25 and 50 mgl-1 of CN- proved lethal. Under stressed conditions, previously non-lethal exposures (60 s and 50 mgl-1) were lethal. Of the physiological end-points, only the liver O2 consumption rate was indicative of previous CN- exposure. Under non-stressed conditions, pulsed exposures at 25 and 50 mgl-1 of CN- for 10 and 60 s significantly reduced the liver O2 consumption rates (ANOVA; p〈0.05). Under stressed conditions, the liver O2 consumption rates were significantly greater (maximum rates up to 17-fold greater) than the control fish (ANOVA; p〈0.05). We conclude, therefore, that environmentally relevant exposures of CN- can adversely effect fish and this affect can be measured 2.5 weeks post-exposure. Importantly, the combined effects of exposure and stress both increased the mortality and placed an appreciable metabolic load on the fish as indicated by the elevated liver O2 consumption rates. Handling stress in combination with anaesthetic CN- doses could in part explain the delayed mortality reportedly associated with CN- use in the tropical fish trade. The significance of the elevated liver O2 consumption rates on the survival of CN--exposed fish is unknown.
    Type of Medium: Electronic Resource
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  • 2
    Electronic Resource
    Electronic Resource
    Springer
    Journal of comparative physiology 164 (1994), S. 438-443 
    ISSN: 1432-136X
    Keywords: Ryanodine ; Sarcoplasmic reticulum ; Temperature ; Acclimation ; Trout,Oncorhynchus mykiss
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Abstract The influence of acute temperature change and temperature acclimation on the sensitivity of contracture development to ryanodine were examined in the rainbow trout myocardium using two preparations: in vitro isolated ventricular strips and in situ working perfused hearts. Ryanodine effects in vitro were dependent on test temperature (8 and 18 °C), pacing frequency (0.2–1.5 Hz) and acclimation temperature (8 and 18 °C). At a pacing frequency of 0.2 Hz and a test temperature of 18 °C, ryanodine depressed isometric tension development in ventricular strips both from trout acclimated to 8 and 18 °C but the decrease was significantly greater in strips from 8 °C-acclimated trout. No ryanodine effect was observed in either acclimation group at a test temperature of 8°C. The effect of ryanodine in vitro was reduced or lost at pacing frequencies greater than 0.2 Hz and at 0.6 Hz ryanodine depressed tension development at 18 °C only in strips from 8 °C-acclimated trout. Ryanodine did not affect tension development at stimulation rates above 0.6 Hz in any test group. Likewise, ryanodine did not significantly impair cardiac performance of in situ working perfused heart preparations which operated at intrinsic beat frequencies in excess of 0.6 Hz. These results suggest that the sarcoplamic reticulum calcium release channel of the trout myocardium is expressed but is not functionally involved in beat-to-beat regulation of contractility at either (1) low temperature (8 °C), or (2) at routine physiological heart rate (〉0.6 Hz). However, under conditions in which involvement of the sarcoplasmic reticulum is observed (18 °C and a heart rate 〈 0.6 Hz), prior acclimation to low temperature results in either a greater capacity of the sarcoplasmic reticulum to store releasable calcium or an increase in the amount of calcium that is in releasable form.
    Type of Medium: Electronic Resource
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