scholarly journals Effect of coronary perfusion on the basal performance, volume loading and oxygen consumption in the isolated resistance-headed heart of the trout Oncorhynchus mykiss

2003 ◽  
Vol 206 (22) ◽  
pp. 4003-4010 ◽  
Author(s):  
C. Agnisola
Keyword(s):  
Oxygen Consumption ◽  
Oncorhynchus Mykiss ◽  
Coronary Perfusion ◽  
Volume Loading ◽  
Performance Volume

Action of adenosine on energetics, protein synthesis and K(+) homeostasis in teleost hepatocytes

2000 ◽  
Vol 203 (17) ◽  
pp. 2657-2665 ◽  
Author(s):  
G. Krumschnabel ◽  
C. Biasi ◽  
W. Wieser
Keyword(s):  
Protein Synthesis ◽  
Oxygen Consumption ◽  
Atpase Activity ◽  
Oncorhynchus Mykiss ◽  
Carassius Auratus ◽  
Goldfish Carassius Auratus ◽  
Inhibition Of Protein Synthesis ◽  
Rate Of Oxygen Consumption ◽  
A1 Receptor ◽  
Lactate Formation

In a comparative study, we analysed the effects of adenosine on the energetics, protein synthesis and K(+)homeostasis of hepatocytes from the anoxia-tolerant goldfish Carassius auratus and the anoxia-intolerant trout Oncorhynchus mykiss. The rate of oxygen consumption did not respond immediately to the addition of adenosine to the cells from either species, but showed a significant decrease in trout hepatocytes after 30 min. The anaerobic rate of lactate formation was not significantly affected by adenosine in goldfish hepatocytes, but was increased in trout cells. We also studied the effects of adenosine on the two most prominent ATP consumers in these cells, protein synthesis and Na(+)/K(+)-ATPase activity. Under aerobic conditions, adenosine inhibited protein synthesis of hepatocytes from goldfish by 51% and of hepatocytes from trout by 32%. During anoxia, the rate of protein synthesis decreased by approximately 50% in goldfish hepatocytes and by 90% in trout hepatocytes, and this decrease was not altered by the presence of adenosine. Adenosine inhibited normoxic Na(+)/K(+)-ATPase activity and K(+)efflux by 20–35% in the cells of both species. An investigation into the mechanism underlying the inhibition of protein synthesis by adenosine indicated that, in the goldfish cells, adenosine acts via a membrane receptor-mediated pathway, i.e. the effect of adenosine was abolished by applying the A1 receptor antagonist 8-phenyltheophylline. In the trout, however, the uptake of adenosine into hepatocytes seems to be required for an effect on protein synthesis. [Ca(2+)](i) does not seem to be involved in the inhibition of protein synthesis by adenosine.

Coronary flow-pressure relationship in the working isolated fish heart: trout (Oncorhynchus mykiss) versus torpedo (Torpedo marmorata)

1994 ◽  
Vol 343 (1304) ◽  
pp. 189-198 ◽  
Keyword(s):  
Coronary Artery ◽  
Coronary Flow ◽  
Filling Pressure ◽  
Coronary Perfusion ◽  
Coronary Resistance ◽  
Volume Loading ◽  
Work Condition ◽  
Input Pressure ◽  
Flow Pressure ◽  
High Work

Isolated hearts of rainbow trout and torpedo were perfused via the atrium and coronary artery under conditions of low and high work and with two different levels of oxygen to determine the effects on coronary flow-pressure relationships and to estimate coronary resistance. In all cases, an increase in input pressure to the coronary artery resulted in an increase in coronary flow through a reduction in coronary resistance. The relationship between flow and pressure was linear but the resistance became less pressure dependent at higher input pressures. When the trout heart was perfused with oxygenated saline an increase in the atrial filling pressure (volume loading, high work condition) reduced coronary resistance and increased flow for a given coronary artery input pressure. The opposite effects were seen when atrial filling pressure was reduced (volume loading, low work condition). Increasing ventricular output pressure (pressure loading) resulted in an increased coronary resistance. In torpedo, changes in preload and afterload did not affect coronary perfusion. In both preparations, reduced levels of oxygen in the coronary perfusion fluid reduced coronary resistance. It is concluded that in trout the coronary resistance is intrinsically sensitive to input pressure and oxygen demand of the ventricle; these susceptibilities assist in the maintenance of the oxygen supply to the compact layer of ventricular muscle. In contrast, the coronary resistance of the torpedo heart appears to be insensitive to load conditions when steady-state perfusion pressure is used. The difference between the two species is discussed in terms of m orphofunctional differences in the coronary system.

Influence of low temperature acclimation on fate of metabolic fuels in rainbow trout (Oncorhynchus mykiss) hearts

1993 ◽  
Vol 71 (11) ◽  
pp. 2167-2173 ◽  
Author(s):  
John R. Bailey ◽  
William R. Driedzic
Keyword(s):  
Oxygen Consumption ◽  
Rainbow Trout ◽  
Oncorhynchus Mykiss ◽  
Temperature Acclimation ◽  
Experimental Conditions ◽  
Intracellular Lipids ◽  
Rainbow Trout Oncorhynchus Mykiss ◽  
Significant Difference ◽  
Precipitate Protein ◽  
Fuel Source

Rainbow trout (Oncorhynchus mykiss) were acclimated to 5 and 20 °C. Oxygen consumption of isolated perfused hearts was measured at 5 or 15 °C with either glucose or palmitate as the exogenous fuel source. With glucose as the fuel there was no significant difference in oxygen consumption of hearts from either acclimation group at either temperature. With palmitate as the fuel source, hearts from fish acclimated to and tested at 5 °C had significantly higher oxygen consumption than hearts from fish acclimated to 20 °C and tested at either 5 or 15 °C. Hearts from fish both acclimated to and tested at 5 °C had a higher oxygen consumption with palmitate than when glucose was supplied. This reflects the preference for fatty acid fuels found in cold acclimated muscle tissue, and consequently the amount of oxygen required to utilize fats. Under all experimental conditions, 14CO2 production from either (6-14C)glucose or (1-14C)palmitate could account for less than 0.5% of oxygen consumption. Tissue chemical analysis showed that most of the label from (6-14C)glucose appeared in acid-soluble (glycolytic intermediates, citric acid cycle intermediates, amino acids, etc.) and lipid fractions while most of the label from (1-14C)palmitate appeared in lipid- or acid-soluble or acid precipitate (protein material) fractions. This indicates considerable dilution of exogenous fuels in endogenous pools, which could account for the discrepancy in measured O2 consumption and 14CO2 production. Glucose catabolism was little affected by either acute or chronic changes in temperature other than an increase in glucose incorporation into the glycogen pool. Hearts from fish both acclimated to and tested at 5 °C showed an increased handling of exogenous fatty acids as reflected by elevated rates of catabolism and incorporation into intracellular lipids.

scholarly journals INFLUENCE OF HYPOXIA AND ADRENALINE ADMINISTRATION ON CORONARY BLOOD FLOW AND CARDIAC PERFORMANCE IN SEAWATER RAINBOW TROUT (ONCORHYNCHUS MYKISS)

1994 ◽  
Vol 193 (1) ◽  
pp. 209-232 ◽  
Author(s):  
A Gamperl ◽  
A Pinder ◽  
R Grant ◽  
R Boutilier
Keyword(s):  
Blood Flow ◽  
Rainbow Trout ◽  
Oncorhynchus Mykiss ◽  
Coronary Blood Flow ◽  
Cardiac Performance ◽  
Hypoxic Exposure ◽  
Coronary Perfusion ◽  
Adrenergic Stimulation ◽  
Rainbow Trout Oncorhynchus Mykiss ◽  
Cardiovascular Performance

To investigate the relationship between cardiac performance and coronary perfusion, cardiovascular variables (Q(dot), Vs, fh, Pda) and coronary blood flow (q·cor) were measured in rainbow trout (Oncorhynchus mykiss) (1.2­1.6 kg) before and after adrenergic stimulation (1.0 µg kg-1 adrenaline) under conditions of (1) normoxia, (2) hypoxia (approximate PwO2 12 kPa) and (3) 2.5 h after returning to normoxia. q·cor for resting fish under normoxic conditions was 0.14±0.02 ml min-1 kg-1 (approximately 0.85 % of Q(dot)). When exposed to hypoxia, although both resting Q(dot) and q·cor increased, q·cor increased to a greater degree (Q(dot) by 17 % and q·cor by 36 %). During hypoxia, maximum adrenaline-stimulated Q(dot) was comparable to that observed for normoxic fish. However, because Q(dot) was elevated in resting hypoxic fish, the capacity of hypoxic fish to increase Q(dot) above resting levels was 50 % lower than that measured in normoxic fish. Although maximum q·cor in adrenaline-injected hypoxic trout was greater than that measured in normoxic trout, post-injection increases in q·cor (above resting levels) were not different between the two groups. Two and a half hours after hypoxic exposure, resting Q(dot) was still elevated (11 %) above normoxic levels, and the ability to increase Q(dot) when adrenergically stimulated was not fully restored. These results suggest (1) that resting q·cor in salmonids is approximately 1 % of Q(dot), (2) that increases in q·cor may be important in maintaining cardiovascular performance during hypoxic conditions, (3) that interactions between alpha-adrenergic constriction and metabolically related vasodilation of the coronary vasculature are important in determining q·cor in fish, (4) that exposure of fish to moderate environmental hypoxia reduces the scope for adrenergically mediated increases in Q(dot), and (5) that periods of recovery in excess of several hours are required before cardiovascular performance returns to pre-hypoxic levels.

scholarly journals Myocardial Oxygen Consumption in the Sea Raven, Hemitripterus Americanus: the Effects of Volume Loading, Pressure Loading And Progressive Hypoxia

1985 ◽  
Vol 117 (1) ◽  
pp. 237-250 ◽  
Author(s):  
A. P. FARRELL ◽  
S. WOOD ◽  
T. HART ◽  
W. R. DRIEDZIC
Keyword(s):  
Oxygen Consumption ◽  
Power Output ◽  
Myocardial Oxygen Consumption ◽  
Mechanical Efficiency ◽  
Pressure Loading ◽  
Volume Loading ◽  
Perfused Heart ◽  
Linear Fashion ◽  
Progressive Hypoxia ◽  
O2 Delivery

1. Myocardial oxygen consumption (VOO2) was measured using an in situ, perfused heart preparation at 10°C. VOO2 increased in a linear fashion with power output when cardiac output (Vb) was elevated (volume loading). The increased VOO2 was possible through improved O2 delivery (increased Vb), but Δ POO2 (input POO2 - output POO2) was reduced. The mechanical efficiency of the heart was improved. 2. VOO2 also increased in a linear fashion with power output when output pressure was increased with Vb constant (pressure loading). The increased VOO2 was supported by increased O2 removal from the perfusate since oxygen delivery (Vb and input POO2) was constant. Once more, improved mechanical efficiency was observed. 3. VOO2 decreased as O2 delivery was reduced with progressive hypoxia. Even so, power output was maintained at a perfusate input POO2 of 81 Torr. Five of 11 hearts survived a 30-Torr POO2 exposure, but with a 29% decrease in power output and a 5-fold reduction in VOO2. The increase in the apparent aerobic efficiency which enabled this is discussed.

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