Ion Flux Rates, Acid–Base Status, and Blood Gases in Rainbow Trout, Salmo gairdneri, Exposed to Toxic Zinc in Natural Soft Water

1985 ◽  
Vol 42 (8) ◽  
pp. 1332-1341 ◽  
Author(s):  
Douglas J. Spry ◽  
Chris M. Wood
Keyword(s):  
Rainbow Trout ◽  
Metabolic Acidosis ◽  
Ammonia Excretion ◽  
Blood Gases ◽  
Soft Water ◽  
Salmo Gairdneri ◽  
Acid Base ◽  
Flux Measurements ◽  
Water Base ◽  
Toxic Concentrations

Exposure to 0.8 mg Zn2+/L in natural soft water for up to 72 h was toxic to rainbow trout, Salmo gairdneri, causing an acid–base disturbance and net branchial ion losses. Mean arterial pH fell from 7.78 to 7.58. Both [Formula: see text] and lactate rose, indicating a mixed respiratory and metabolic acidosis, despite maintenance of high [Formula: see text] Net branchial uptake of Na+ and Cl− became a net loss immediately following exposure to Zn2+, and this continued during 60 h of exposure. Net K+ loss was exacerbated, and net Ca2+ uptake was abolished. Unidirectional flux measurements with 22Na+ and 36Cl− indicated an increased efflux immediately following zinc exposure. Both influx and efflux of Na+ and Cl− were stimulated after 48–60 h in Zn2+. Both net branchial ammonia excretion and net branchial uptake of acidic equivalents from the water (=base loss) were greatly stimulated, the latter contributing to metabolic acidosis. Kidney function, as measured by urine flow rate and excretion of ammonia, acidic equivalents, Na+, Cl−, K+, and Zn2+, was relatively insensitive to the effects of zinc. The only renal component to be affected was Ca2+ excretion, which decreased during a single flux period, possibly in response to the reduced entry of Ca2+ at the gill. We conclude that toxic concentrations of zinc are capable of altering gill function so as to cause ionoregulatory and acid–base disturbances without disturbance of [Formula: see text].

Long-Term Sublethal Acid Exposure in Rainbow Trout (Salmo gairdneri) in Soft Water: Effects on Ion Exchanges and Blood Chemistry

1988 ◽  
Vol 45 (8) ◽  
pp. 1387-1398 ◽  
Author(s):  
Céline Audet ◽  
R. Stephen Munger ◽  
Chris M. Wood
Keyword(s):  
Rainbow Trout ◽  
Ammonia Excretion ◽  
Blood Chemistry ◽  
Soft Water ◽  
Acid Exposure ◽  
Salmo Gairdneri ◽  
Plasma Parameters ◽  
Water Effects ◽  
Net Flux

Long-term sublethal acid exposure (3 mo, pH 4.8) in adult rainbow trout (Salmo gairdneri) acclimated to artificial soft water (Ca2+ = 50, Na+ = 50, Cl− = 100 μeq∙L−1) caused transient net fosses of Na+ and Cl−. Net flux rates of both ions were returned to control levels after 30–52 d of acid exposure through a new equilibrium between unidirectional influx and efflux, where both were lower than control rates. K+ balance remained negative and Ca2+ balance at zero throughout the exposure. No changes in net acidic equivalent flux occurred, indicating the absence of acid–base disturbance, but ammonia excretion increased over time. Muscle K+, Na+, and Cl− fell and Ca2+ increased. Plasma Na+, Cl−, and osmolality decreased, while plasma protein, glucose, and blood hemoglobin increased during the first few weeks of acid exposure. Plasma K+ and Ca2+ did not change. General stabilization of plasma parameters occurred in concert with the stabilization of Na+ and Cl− flux rates, but no recovery to control levels was observed for any of them. We conclude that despite this stabilization at a new steady state, rainbow trout were physiologically affected in a deleterious manner by chronic sublethal acid exposure in soft water.

Branchial mechanisms of ion and acid–base regulation in the freshwater rainbow trout, Salmo gairdneri

1988 ◽  
Vol 66 (12) ◽  
pp. 2699-2708 ◽  
Author(s):  
D. G. McDonald ◽  
E. T. Prior
Keyword(s):  
Lactic Acid ◽  
Rainbow Trout ◽  
Sodium Bicarbonate ◽  
Ammonium Sulphate ◽  
Ammonia Excretion ◽  
Salmo Gairdneri ◽  
Acid Base Balance ◽  
Acid Base ◽  
Base Balance

Blood acid–base balance and branchial fluxes of Na+, Cl−, and acidic equivalents were examined in rainbow trout (Salmo gairdneri) in response to variations in external [NaCl] and following experimental acid or base loads (intravascular infusion of ammonium sulphate, lactic acid, or sodium bicarbonate). NaCl influx, NaCl efflux, and ammonia excretion covaried with external [NaCl]. Large fluxes of acidic equivalents across the gills were produced by infusion of both ammonium sulphate and sodium bicarbonate, but both treatments had little effect upon Na+ and Cl− uptake. We interpret this result as indicating that apical [Formula: see text] and [Formula: see text] exchange played little role in the branchial clearance of acidic equivalents. Instead, the results are consistent with the notion that acidic equivalents were excreted via diffusion through paracellular channels. A model is presented which suggests that the paracellular channels are the normal route for ionic efflux across the gills and that excretion of acidic equivalents results from modulation of the permselectivity of this pathway.

scholarly journals The effects of prolonged epinephrine infusion on the physiology of the rainbow trout, Salmo gairdneri. II. Branchial solute fluxes

1987 ◽  
Vol 128 (1) ◽  
pp. 255-267 ◽  
Author(s):  
M. G. Vermette ◽  
S. F. Perry
Keyword(s):  
Rainbow Trout ◽  
Ammonia Excretion ◽  
Salmo Gairdneri ◽  
Ionic Exchange ◽  
Acid Base ◽  
Epinephrine Infusion ◽  
Extracellular Acidosis ◽  
Titratable Acid ◽  
Solute Fluxes ◽  
Circulating Levels

Rainbow trout were infused continuously for 24 h with epinephrine in order to elevate circulating levels to those measured during periods of acute extracellular acidosis (about 5 X 10(−8) mol l-1). Concomitant effects on branchial solute fluxes were evaluated. Epinephrine infusion caused complex and differential adjustments of Na+ and Cl- unidirectional fluxes (influx and efflux) resulting in a significant elevation of the arithmetic difference between Na+ and Cl- net fluxes (JnetNa+-JnetCl-). A significant correlation existed between JnetNa+-JnetCl- and net branchial acid excretion (JnetH+), thereby suggesting a role for epinephrine in piscine acid-base regulation. The stimulation of JnetH+ by epinephrine was due primarily to a reduction in the excretion of titratable acid (JTA) accompanied by non-significant changes in ammonia excretion (JAmm). The results are discussed with respect to a role for epinephrine in regulating acid-base disturbances by interacting with branchial ionic exchange mechanisms.

Adrenergic Regulation of Blood Acid-Base Status following Exhaustive Exercise in Seawater-Adapted Rainbow Trout, Salmo gairdneri

1989 ◽  
Vol 62 (4) ◽  
pp. 950-963 ◽  
Author(s):  
Y. Tang ◽  
D. G. McDonald ◽  
R. G. Boutilier
Keyword(s):  
Rainbow Trout ◽  
Exhaustive Exercise ◽  
Salmo Gairdneri ◽  
Acid Base ◽  
Adrenergic Regulation ◽  
Acid Base Status

Respiratory, Ventilatory, Acid-Base and Ionoregulatory Physiology of the White Sucker Catostomus Commersoni: The Influence of Hyperoxia

1981 ◽  
Vol 91 (1) ◽  
pp. 239-254
Author(s):  
P. R. H. Wilkes ◽  
R. L. Walker ◽  
D. G. McDonald ◽  
C. M. Wood
Keyword(s):  
Rainbow Trout ◽  
Blood Gases ◽  
Catostomus Commersoni ◽  
Acid Base ◽  
Aortic Blood ◽  
Respiratory Parameters ◽  
Arterial Ph ◽  
O2 Extraction ◽  
Acid Base Status ◽  
Aortic Blood Pressure

Blood gases, acid-base status, plasma ions, respiration, ventilation and cardiovascular function were measured in white suckers, using standard cannulation methods. Basic respiratory parameters under normoxia were compared to those in the active, pelagic rainbow trout and in other benthic teleosts. Sustained environmental hyperoxia (350–550 torr) increased arterial O2 (102–392 torr) and venous O2 (17–80 torr) tensions so that blood O2 transport occurred entirely via physical solution. Dorsal aortic blood pressure and heart rate fell, the latter due to an increase in vagal tone. Ventilation volume declined markedly (by 50%) due to a decrease in ventilatory stroke volume, but absolute O2 extraction rose so that O2 consumption was unaffected. While the preceding effects were stable with time, arterial and venous CO2 tensions approximately doubled within 4 h, and continued to increase gradually thereafter. This CO2 retention caused an acidosis (7.993–7.814) which was gradually compensated by an accumulation of plasma [HCO3−]. However, even after 72 h, arterial pH remained significantly depressed by 0.10 units. The gradual rise in plasma [HCO3−] was accompanied by a progressive fall in both [Na+] and [Cl−]; [K+] and [Ca2+] remained unchanged. The responses of the sucker to hyperoxia are compared to those of the rainbow trout.

Acid-Base Regulation Following Exhaustive Exercise: A Comparison Between Freshwaterand Sea Water-Adapted Rainbow Trout (Salmo Gairdneri)

1989 ◽  
Vol 141 (1) ◽  
pp. 407-418 ◽  
Author(s):  
Y. TANG ◽  
D. G. McDONALD ◽  
R. G. BOUTILIER
Keyword(s):  
Rainbow Trout ◽  
Sea Water ◽  
Environmental Water ◽  
Exhaustive Exercise ◽  
Salmo Gairdneri ◽  
Acid Base ◽  
Genetic Stock ◽  
Arterial Blood ◽  
Blood Ph ◽  
Counter Ions

Blood acid-base regulation following exhaustive exercise was investigated in freshwater- (FW) and seawater- (SW) adapted rainbow trout (Salmo gairdneri) of the same genetic stock. Following exhaustive exercise at 10°C, both FW and SW trout displayed a mixed respiratory and metabolic blood acidosis. However, in FW trout the acidosis was about double that of SW trout and arterial blood pH took twice as long to correct. These SW/FW differences were related to the relative amounts of net H+ equivalent excretion to the environmental water, SW trout excreting five times as much as FW trout. The greater H+ equivalent excretion in SW trout may be secondary to changes in the gills that accompany the adaptation from FW to SW. It may also be related to the higher concentrations of HCO3− as well as other exchangeable counter-ions (Na+ and Cl−) in the external medium in SW compared to FW.

Acute Ammonia Toxicity and Ammonia Excretion in Rainbow Trout (Salmo gairdneri)

1979 ◽  
Vol 36 (6) ◽  
pp. 621-629 ◽  
Author(s):  
Betty A. Hillaby ◽  
David J. Randall
Keyword(s):  
Rainbow Trout ◽  
Ammonia Excretion ◽  
Hydrogen Ion ◽  
Ammonia Toxicity ◽  
Salmo Gairdneri ◽  
Mean Values ◽  
Arterial Blood ◽  
Blood Ph ◽  
Before And After ◽  
Total Ammonia

Acute ammonia toxicity in rainbow trout (Salmo gairdneri) was studied by intraarterial injection of NH4Cl and NH4HCO3. Hydrogen ion and total ammonia concentrations were measured in blood sampled from the dorsal aorta both before and after injection. Although injection of NH4HCO3 increased arterial blood pH, and injection of NH4Cl decreased arterial blood pH, the same dose of each was required to kill fish. While the un-ionized form of ammonia in water has been shown to be toxic, in the blood either the ionized form or the total ammonia load is toxic to fish. Ammonia levels were measured in pre- and postbranchial blood. Mean values were not significantly different, but paired values indicated a fall in blood ammonia due to excretion across the gills. There appears to be a more rapid excretion of ammonia following NH4HCO3 infusions, which result in higher un-ionized ammonia levels in blood compared with those following NH4Cl infusions. These results are consistent with the hypothesis that ammonia is excreted in the un-ionized form. Key words: un-ionized ammonia, ionized ammonia, gills, pH, blood

Blood acid-base regulation during environmental hyperoxia in the rainbow trout (Salmo gairdneri)

1980 ◽  
Vol 42 (3) ◽  
pp. 351-372 ◽  
Author(s):  
Chris M. Wood ◽  
Eric B. Jackson
Keyword(s):  
Rainbow Trout ◽  
Salmo Gairdneri ◽  
Acid Base

Models of Ammonia Excretion for Brook Trout (Salvelinus fontinalis) and Rainbow Trout (Salmo gairdneri)

1980 ◽  
Vol 37 (9) ◽  
pp. 1421-1425 ◽  
Author(s):  
Larry J. Paulson
Keyword(s):  
Body Weight ◽  
Rainbow Trout ◽  
Brook Trout ◽  
Salvelinus Fontinalis ◽  
Ammonia Excretion ◽  
Salmo Gairdneri ◽  
Feeding Rates ◽  
Data Set ◽  
Nitrogen Consumption ◽  
Good Agreement

Ammonia excretion by brook trout (Salvelinus fontinalis) and rainbow trout (Salmo gairdneri) was measured in relation to nitrogen consumption, body weight (15–154 g for rainbow trout and 50–360 g for brook trout), and temperature (11.2–21.0 °C) under laboratory conditions. Four natural diets, collected from Castle Lake, California, and a commercial pellet diet were fed to the trout in gelatin capsules at feeding rates from 2.5 to 5% body weight∙d−1. Nitrogen consumption was the most important factor influencing ammonia excretion, followed by body weight and temperature. Testing the models with an independent data set revealed good agreement between measured and predicted rates of excretion. The models seem to estimate adequately ammonia excretion by trout in both natural and artificial aquatic systems.Key words: models, ammonia excretion, nitrogen consumption, body weight, temperature, multiple regression, rainbow trout, brook trout

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