Turnover and Urinary Excretion of Free and Acetylated M.S. 222 by Rainbow Trout, Salmo gairdneri

1968 ◽  
Vol 25 (1) ◽  
pp. 25-31 ◽  
Author(s):  
Joseph B. Hunn ◽  
Richard A. Schoettger ◽  
Wayne A. Willford

Rainbow trout: (Salmo gairdneri) anesthetized in 100 mg/liter of M.S. 222 at 12 C excreted the drug in free and acetylated forms via the urine during a 24-hr recovery period in freshwater. Of the M.S. 222 excreted, 77–96% was acetylated. Blood levels of free drug in anesthetized trout approximated 75% of the anesthetic concentration, but the amount of acetylated M.S. 222 was relatively insignificant. The blood and urine were cleared of the two fractions of M.S. 222 in 8 and 24 hr respectively. Low levels of aromatic amines of natural origin occurred in blood and urine and were subtracted from measurements of M.S. 222. Intraperitoneal injections of 10–100 mg/kg of M.S. 222 did not induce anesthesia; however, the 24-hr pattern of drug excretion was similar to that observed after anesthesia by immersion. Only 15–21% of the injected dose was found in the urine, suggesting a second route of drug elimination.

1983 ◽  
Vol 104 (1) ◽  
pp. 247-268 ◽  
Author(s):  
JEFFREY D. TURNER ◽  
CHRIS M. WOOD ◽  
DONNA CLARK

Chronically cannulated rainbow trout were subjected to 6 min of severe burst exercise and monitored over a 12 h recovery period. There were short-lived increases in haematocrit, haemoglobin, plasma protein, Na+ and Cl− levels. Plasma [Cl−] later declined below normal as organic anions accumulated. A much larger and more prolonged elevation in plasma [K+] probably resulted from intracellular acidosis. An intense extracellular acidosis was initially of equal respiratory (i.e. Pa,COa,CO2) a nd metabolic (i.e. ΔH+m) origin. However Pa,COa,CO2 was rapidly corrected while the metabolic component persisted. Plasma ammonia increases had negligible influence on acid-base status. Elevations in blood lactate (ΔLa−) were equal to ΔH+m immediately post-exercise but later rose to twice the latter. Simultaneous white muscle biopsies and blood samples demonstrated that muscle to blood gradients of lactate and pyruvate were maximal immediately post-exercise. As blood levels rose and muscle levels declined, an approximate equilibrium was reached after 4 h of recovery. Intra-arterial infusions of lactic acid in resting trout produced a severe but rapidly corrected metabolic acidosis. The rates of disappearance of ΔH+m and ΔLa− from the blood were equal. Infusions of similar amounts of sodium lactate produced a small, prolonged metabolic alkalosis with a much slower ΔLa− disappearance rate. It is suggested that the excess of ΔLa− over ΔH+m in the blood after exercise is associated with differential release rates of the two species from white muscle rather than differential removal rates from the bloodstream, and that the majority of the lactic acid load in muscle is removed by metabolism in situ.


1976 ◽  
Vol 33 (1) ◽  
pp. 173-176 ◽  
Author(s):  
William R. Driedzic ◽  
Joe W. Kiceniuk

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.


1981 ◽  
Vol 45 (1) ◽  
pp. 137-148 ◽  
Author(s):  
D. Knox ◽  
C. B. Cowey ◽  
J. W. Adron

1. Rainbow trout (Salmo gairdneri) of mean initial weight 35 g were given one of five experimental diets for 20 weeks. The diets contained (g/kg dry diet) 15 calcium, 10 phosphorus and graded levels of magnesium from 0.04 (diet no. 1) to 1.0 (diet no. 5). In a second experiment rainbow trout of mean initial weight 16 g were given one of six experimental diets for 20 weeks. The diets contained (g/kg dry diet): Ca (40), P (30) and levels of Mg from 0.06 (diet no. 6) to 2.0 (diet no. 11).2. In both experiments weight gains were lowest in those trout given diets containing the basal levels of Mg (diet no. 1 and diet no. 6) but increased with increasing dietary Mg concentration. In neither experiment was there any further increase in weight gain once the Mg concentration reached 0.25–0.5 g/kg dry diet; weight gain reached a plateau at this dietary Mg level.3. The following trends occurred in serum electrolyte concentrations as dietary Mg increased. Mg increased in both experiments, in Expt 2 it reached a maximum of 1 mmol/l when the diet containted 0.5 g Mg/kg and did not increase further; sodium was positively correlated in both experiments; potassium decreased and in Expt 2 reached a plateau minimum of 1.7 mmol/l at a dietary Mg concentration of 0.5 g/kg; Ca and P altered little in either experiment.4. In both experiments renal Ca concentrations were greatly increased in trout given diets lacking supplementary Mg; they fell to low levels (3–5 mmol/kg) when diets conained 0.15 g Mg/kg or more. Renal K and P concentrations were negatively correlated with dietary Mg in Expt 2; other electrolytes measured were not altered in concentration by the treatments used.5. Extracellular fluid volume (ECFV) of muscle was negatively correlated with dietary Mg. In Expt 2 it reached a minimal or normal value at 0.5 g Mg/kg diet and did not decease further. Muscle Mg concentration increased with diet Mg in both experiments and muscle K concentration was also correlated with diet Mg in Expt 2. These changes were related to the shift in muscle water. In Expt 1, P concentration was decreased with increasing diet Mg but in Expt 2 its concentration increased, these changes may have been connected with the three-fold difference in dietary P in the two experiments.6. By contrast with skeletal muscle, Mg levels in cardiac muscle increased at low dietary Mg intakes.7. Concentrations of electrolytes in liver did not alter with dietary treatments used.8. The results show that Mg requirement of rainbow trout is met by a diet containing 0.5 g Mg/kg diet.


1985 ◽  
Vol 63 (9) ◽  
pp. 982-987 ◽  
Author(s):  
Jean Louis Maitre ◽  
Catherine Le Guellec ◽  
Stephane Derrien ◽  
Martin Tenniswood ◽  
Yves Valotaire

The study of the seasonal regulation of vitellogenesis in rainbow trout (Salmo gairdneri) is hampered by two features of the system which are not seen in species such as Xenopus. First, it is impossible to sex immature trout by external appearance and, secondly, the quantitation of the very low levels of vitellogenin in previtellogenic serum is technically difficult and tedious. We describe the preparation of a specific, sensitive anti-vitellogenin antibody and the use of this antibody in a rocket immunoelectrophoresis system to measure serum vitellogenin. The sensitivity of the assay is such that, using only 2 μL of serum, it is possible to detect vitellogenin at levels of 10 μg/mL, making this assay extremely useful for selecting immature female trout for further studies on the basis of the presence of vitellogenin. Using this system we have also measured the response of individual male trout to stimulation with different levels of estradiol, and we have shown that it is possible to measure the stimulation of vitellogenin by estradiol levels equivalent to those seen during the previtellogenic phase of the reproductive cycle in females. This simple assay system thus alleviates two of the major hurdles in studying vitellogenesis in trout.


1983 ◽  
Vol 105 (1) ◽  
pp. 1-14
Author(s):  
PETER NEUMANN ◽  
GEORGE F. HOLETON ◽  
NORBERT HEISLER

Rainbow trout (Salmo gairdneri) were electrically stimulated to exhausting activity and the changes in cardiac output and blood flow distribution to gills and systemic tissues resulting from the developing severe lactacidosis were repeatedly measured by the microsphere method (15 μm). Determination of cardiac output by application of the Fick principle resulted in values not significantly different from cardiac output measured by the indicator dilution technique, suggesting that cutaneous respiration, oxygen consumption, and arterio-venous shunting were insignificant under these conditions. Following muscular activity, cardiac output was elevated by up to 60%. In the gills, the blood flow distribution in the gill arches showed a consistent pattern, even during lactacidosis, with a higher perfusion in gill arches II and III, and in the middle sections of individual gills. Blood flow to white and red muscle was increased much more than cardiac output (+230 and +490%, respectively) such that blood flow to other tissues was actually reduced. We conclude that the elimination of lactate from muscle cells during the recovery period from strenuous exercise is delayed, not as a result of an impaired post-exercise muscle blood flow, but probably as a result of a high diffusion resistance in the cell membrane. Note: Deceased.


1983 ◽  
Vol 104 (1) ◽  
pp. 269-288 ◽  
Author(s):  
JEFFREY D. Turner ◽  
CHRIS M. WOOD ◽  
HELVE HÖBE

Chronically cannulated flathead sole were subjected to 10 min of either moderate or exhausting burst exercise and monitored over a 12 h recovery period. Acid-base disturbances were more severe after exhausting exercise, but ionic and haematological changes were the same in the two treatments. Most effects were qualitatively similar to those previously described in severely exercised rainbow trout (Turner, Wood & Clark, 1983). Specific differences are discussed and related to the different external environments sea water vs fresh water), exercise capabilities and ecologies of the two species. The most striking divergence occurred in lactate (La−) and metabolic proton dynamics. Post-exercise La− levels in white muscle in sole were less than half those in trout but declined much more slowly. In contrast to the situation in trout, muscle [La−] remained significantly elevated and large muscle to blood La− gradient persisted even after 12 h recovery. Blood [La−] underwent only minimal elevation (<2 mequiv 1−1), and blood metabolic proton load (ΔH+m) greatly exceeded Δ;La− throughout the recovery period, effects directly opposite those in trout. This observed excess of ΔH+m over ΔLa− in the blood of exercised sole is probably not due to a preferential removal mechanism, because ΔH+m and ΔLa− disappeared from the blood at similar rates after an intra-arterial infusion of lactic acid in resting animals. It is therefore argued that the phenomenon reflects a differential release of the two metabolites from the white muscle of the sole, La− being strictly retained in the muscle for gluconeogenesis in situ.


1986 ◽  
Vol 123 (1) ◽  
pp. 145-157
Author(s):  
R. G. Boutilier ◽  
G. K. Iwama ◽  
D. J. Randall

A fall in blood pH was generated either by infusion of HCl or by reducing gill ventilation and raising blood PCO2 in rainbow trout, Salmo gairdneri Richardson. The acute acidosis resulting from HCl infusion caused an increase in plasma adrenaline and noradrenaline concentrations, the adrenaline increase being proportional to the decrease in blood pH. Fish subjected to a prolonged respiratory acidosis, caused by a reduction in gill ventilation, showed no increase in catecholamines 24 h after the change in gill ventilation. We suggest that catecholamine levels increase in response to a pH decrease, but if acidotic conditions are maintained, circulating catecholamines return to low levels. There was a much smaller decrease in erythrocytic pH with a fall in plasma pH when catecholamine levels were high. This ameliorating effect of catecholamines on erythrocytic pH during a plasma acidosis maintains the oxygen-carrying capacity of the haemoglobin. If erythrocytic pH was decreased by increasing blood PCO2 in vitro, then there was a fall in haemoglobin oxygen-carrying capacity which was proportional to the reduction in pH. We conclude that catecholamines are released into the blood in proportion to the fall in blood pH but if the pH is maintained the circulating catecholamines return to their initial low levels. The elevated catecholamine concentrations in blood safeguard against any impairment of haemoglobin oxygen-carrying capacity by maintaining erythrocytic pH in the face of a plasma acidosis.


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