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

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.

Ammonia toxicity mechanism in fish: Studies on rainbow trout (Salmo gairdneri Rich.)

1981 ◽  
Vol 5 (3) ◽  
pp. 316-328 ◽  
Author(s):  
A. Arillo ◽  
C. Margiocco ◽  
F. Melodia ◽  
P. Mensi ◽  
G. Schenone
Keyword(s):  
Rainbow Trout ◽  
Ammonia Toxicity ◽  
Salmo Gairdneri ◽  
Toxicity Mechanism

Slow postcapillary pH changes in blood in anesthetized animals

1978 ◽  
Vol 45 (5) ◽  
pp. 674-680 ◽  
Author(s):  
A. Bidani ◽  
E. D. Crandall
Keyword(s):  
Blood Cells ◽  
Ph Change ◽  
Arterial Blood ◽  
Blood Ph ◽  
Pulmonary Capillary ◽  
Before And After ◽  
Equilibration Process ◽  
Contact Surfaces ◽  
Electrode Chamber

To investigate the hypothesis that blood pH and PCO2 continue to change after the blood leaves an exchange capillary, we used a rapidly responding, pressure-insensitive, stopped-flow pH electrode apparatus. Arterial blood from an anesthetized dog or cat is drawn through the apparatus into a syringe. Syringe movement is then suddenly stopped. Temperature and pH of the blood in the electrode assembly are continuously monitored, both before and after blood withdrawal ceases. Hemolysis was reduced by coating all blood contact surfaces with silicone and fasting the animal overnight, anesthetizing it with crystalline pentobarbital sodium, and allowing it to ventilate spontaneously. After stopping withdrawal, pH of blood in the electrode chamber continued to change, rising 0.01 unit with t1/2 of 4.4 s. After lysed blood was returned to the animal to provide carbonic anhydrase to the plasma, no pH change was seen after stopping the flow. The small pH rise occurring in arterial blood in vivo is probably due in large part to disequilibrium of [H+] between red blood cells and plasma at the end of the pulmonary capillary, the equilibration process being rate-limited by the extracellular CO2 hydration-dehydration reaction.

Adrenocortical response during corrected and uncorrected hypercapnic acidosis

1962 ◽  
Vol 202 (2) ◽  
pp. 334-336 ◽  
Author(s):  
Arnold Mittelman ◽  
Serge J. Dos ◽  
Harold G. Barker ◽  
Gabriel G. Nahas
Keyword(s):  
Flow Rate ◽  
Venous Blood ◽  
Concomitant Administration ◽  
Cortisol Secretion ◽  
Hypercapnic Acidosis ◽  
Sharp Reduction ◽  
Venous Flow ◽  
Arterial Blood ◽  
Blood Ph ◽  
Before And After

Adrenal venous flow rate and cortisol synthesis have been measured in dogs subjected to hypercapnic acidosis before and after intravenous administration of 0.34 mm/kg of tris (hydroxymethyl) amino methane (THAM). A comparison was made of adrenal venous, peripheral venous, and arterial blood, pH, pCO2 and O2 saturation. During uncorrected hypercapnic acidosis the concentration of cortisol increased while adrenal venous flow rate decreased, but there was a significant increase in the minute output of cortisol. With the concomitant administration of 0.34 mM/kg THAM, adrenal venous flow rate doubled. However, since this enhanced flow rate was accompanied by a sharp reduction in cortisol secretion, the minute output of cortisol returned to control levels. The possibility of a direct effect of THAM on the adrenal vascular bed and synthetic processes is discussed. Throughout all the above experiments adrenal venous blood resembled arterial blood rather than peripheral blood in its pCO2, O2 saturation and pH.

Alveolar hypercapnia augments pulmonary C-fiber responses to chemical stimulants: role of hydrogen ion

2002 ◽  
Vol 93 (1) ◽  
pp. 181-188 ◽  
Author(s):  
Qihai Gu ◽  
Lu-Yuan Lee
Keyword(s):  
Hydrogen Ion ◽  
Right Atrial ◽  
Mechanical Stimuli ◽  
Hydrogen Ions ◽  
Lung Inflation ◽  
C Fibers ◽  
Arterial Blood ◽  
Blood Ph ◽  
C Fiber

To determine whether the excitabilities of pulmonary C fibers to chemical and mechanical stimuli are altered by CO2-induced acidosis, single-unit pulmonary C-fiber activity was recorded in anesthetized, open-chest rats. Transient alveolar hypercapnia (HPC) was induced by administering CO2-enriched gas mixture (15% CO2, balance air) via the respirator inlet for 30 s, which rapidly lowered the arterial blood pH from a baseline of 7.40 ± 0.01 to 7.17 ± 0.02. Alveolar HPC markedly increased the responses of these C-fiber afferents to several chemical stimulants. For example, the C-fiber response to right atrial injection of the same dose of capsaicin (0.25–1.0 μg/kg) was significantly increased from 3.07 ± 0.70 impulses/s at control to 8.48 ± 1.52 impulses/s during HPC ( n = 27; P < 0.05), and this enhanced response returned to control within ∼10 min after termination of HPC. Similarly, alveolar HPC also induced significant increases in the C-fiber responses to right atrial injections of phenylbiguanide (4–8 μg/kg) and adenosine (0.2 mg/kg). In contrast, HPC did not change the response of pulmonary C fibers to lung inflation. Furthermore, the peak response of these C fibers to capsaicin during HPC was greatly attenuated when the HPC-induced acidosis was buffered by infusion of bicarbonate (1.36–1.82 mmol · kg−1 · min−1 for 35 s). In conclusion, alveolar HPC augments the responses of these afferents to various chemical stimulants, and this potentiating effect of CO2 is mediated through the action of hydrogen ions on the C-fiber sensory terminals.

Circulatory and Ventilatory Responses of Rainbow Trout (Salmo gairdneri) to Artificial Manipulation of Gill Surface Area

1971 ◽  
Vol 28 (10) ◽  
pp. 1609-1614 ◽  
Author(s):  
John C. Davis
Keyword(s):  
Blood Flow ◽  
Cardiac Output ◽  
Rainbow Trout ◽  
Surface Area ◽  
Salmo Gairdneri ◽  
Ventilatory Responses ◽  
Arterial Blood ◽  
Gill Area ◽  
Gill Surface Area ◽  
The Brain

Reductions in surface area of the gill were artificially produced by ligating various gill arches and occluding their blood supply. Rainbow trout (Salmo gairdneri) responded to a 40–57% reduction in gill area, by increasing cardiac output and ventilation volume, and probably by redistributing blood within the remaining functional gill area. Fish with blood flow to gill arches one and three only, could maintain arterial PO2 at 90–100 mm Hg, whereas, in those with blood flow to arches three and four only, arterial PO2 fell to around 40 mm Hg. The presence of a chemoreceptor site for the regulation of arterial PO2 associated with the efferent blood vessels of arch number one is discussed. Such a receptor may be located in the pseudobranch or in the portion of the brain supplied with arterial blood from the first gill arch.

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

Blood Lactate Levels in Free-Swimming Rainbow Trout (Salmo gairdneri) Before and After Strenuous Exercise Resulting in Fatigue

1976 ◽  
Vol 33 (1) ◽  
pp. 173-176 ◽  
Author(s):  
William R. Driedzic ◽  
Joe W. Kiceniuk
Keyword(s):  
Rainbow Trout ◽  
Blood Lactate ◽  
White Muscle ◽  
Recovery Period ◽  
Lactate Concentration ◽  
Blood Lactate Concentration ◽  
Strenuous Exercise ◽  
Salmo Gairdneri ◽  
Before And After ◽  
Lactate Levels

Rainbow trout (Salmo gairdneri) were exercised to fatigue in a series of 60-min stepwise increasing velocity increments. There was no increase in blood lactate concentration, serially sampled during swimming by means of indwelling dorsal and ventral aortic catheters, at velocities as high as 93% of critical velocity of individuals. The data show that under these conditions the rate of production of lactate by white muscle, at less than critical velocities, is minimal or that the rate of elimination of lactate from white muscle is equal to its rate of utilization elsewhere. Immediately following fatigue blood lactate level increases rapidly. During the recovery period there appears to be a net uptake of lactate by the gills.

Slow postcapillary changes in blood pH in vivo: titration with acetazolamide

1978 ◽  
Vol 45 (4) ◽  
pp. 565-573 ◽  
Author(s):  
A. Bidani ◽  
E. D. Crandall
Keyword(s):  
Carbonic Anhydrase ◽  
Transport Processes ◽  
Arterial Blood ◽  
Blood Ph ◽  
Pulmonary Capillaries ◽  
Before And After ◽  
Time Courses ◽  
Electrode Chamber ◽  
Good Agreement

A stopped-flow pH electrode apparatus was used to investigate the mechanisms underlying slow changes in plasma pH (pHO) after blood leaves the pulmonary capillaries in carbonic anhydrase-inhibited animals. After acetazolamide was administered to an anesthetized dog or cat, arterial blood was withdrawn through the electrode apparatus into a syringe. Syringe movement was then suddenly stopped. Temperature and pHO of the blood in the electrode chamber were monitored both before and after blood withdrawal ceased. After stopping flow, pHO of the blood in the electrode chamber a) rose 0.02 after a dose of about 1 mg/kg acetazolamide; b) did not change after a dose of about 2 mg/kg acetazolamide; and c) fell 0.10 after a dose greater than about 5 mg/kg acetazolamide. With reasonable red cell and plasma carbonic anhydrase activities assumed for each dose level of acetazolamide, a computer model of the reaction and transport processes occurring in blood after gas exchange in the lung yielded predicted time courses of pHo that were in good agreement with the experimental results. The observed slow pHo changes are largely a result of disequilibrium of [H+] between red blood cells and plasma as blood leaves the pulmonary capillaries.

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