Effects of swimming and environmental hypoxia on coronary blood flow in rainbow trout

1995 ◽  
Vol 269 (5) ◽  
pp. R1258-R1266 ◽  
Author(s):  
A. K. Gamperl ◽  
M. Axelsson ◽  
A. P. Farrell
Keyword(s):  
Blood Flow ◽  
Rainbow Trout ◽  
Coronary Blood Flow ◽  
Swimming Speed ◽  
Power Output ◽  
Cardiac Performance ◽  
Coronary Perfusion ◽  
Cardiac Power ◽  
Rainbow Trout Oncorhynchus Mykiss ◽  
Aortic Blood Pressure

Previous studies have suggested that trout cardiac performance is highly dependent on coronary blood flow during periods of increased activity or hypoxia. To examine the relationship between coronary perfusion and cardiac performance in swimming trout, cardiac output (Q), coronary blood flow (qcor), and dorsal aortic blood pressure were measured in rainbow trout (Oncorhynchus mykiss) during normoxia and hypoxia (PO2 approximately 9 kPa). In normoxic trout, stepwise changes in cardiovascular variables were observed as the swimming speed was incrementally increased from 0.15 body lengths (bl)/s to 1.0 bl/s. At 1.0 bl/s, qcor and cardiac power output had both increased by approximately 110%, and coronary artery resistance (Rcor) had decreased by 40%. During hypoxia, resting qcor was 35% higher, and Rcor was 20% lower, compared with normoxic values. In hypoxic swimming trout, the maximum changes in qcor (155% increase) and Rcor (50% decrease) were recorded at 0.75 bl/s. In contrast, cardiac power output and Q increased by an additional 40 and 20%, respectively, as swimming speed was increased from 0.75 to 1.0 bl/s. The results indicate that 1) increases in qcor parallel changes in cardiac power output; 2) during hypoxia there are compensatory increases in cardiac performance and coronary perfusion; and 3) the scope for increasing qcor in swimming trout is approximately 150%. In addition, results from preliminary experiments suggest that beta-adrenergic, but not cholinergic, mechanisms are involved in the regulation of coronary blood flow during exercise.

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 Sexual Maturity Can Double Heart Mass and Cardiac Power Output in Male Rainbow Trout

1992 ◽  
Vol 171 (1) ◽  
pp. 139-148 ◽  
Author(s):  
CRAIG E. FRANKLIN ◽  
PETER S. DAVIE
Keyword(s):  
Rainbow Trout ◽  
Body Mass ◽  
Power Output ◽  
Cardiac Performance ◽  
Mature Male ◽  
Perfused Heart ◽  
Cardiac Power ◽  
Heart Preparation ◽  
Ovary Growth

Mature male rainbow trout have significantly higher relative ventricle masses (RVM, ventricle mass as a percentage of body mass) than do immature males or females. Hatchery-reared maturing male trout had a mean RVM of 0.139%, whereas females had an RVM of only 0.074 %. Moreover, as males matured and their testes grew from 0.07 to 3.92 % of body mass, RVM more than doubled. In female trout no such heart growth occurred; RVM remained unchanged during the period of ovary growth. Cardiac performance was assessed using an in situ perfused heart preparation. Mature male trout have larger ventricles and could generate significantly greater maximum cardiac power output per kilogram body mass than could immature males or females. This enhanced cardiac performance by the mature males was attributable to delivery of greater cardiac outputs (through larger stroke volumes) and an increased ability of the heart to work against higher output pressures. Power output per gram ventricle mass was similar in both sexes. Note: Present address: Department of Zoology, University of Queensland, Brisbane 4072, Australia.

Contribution of extravascular compression to reduction of maximal coronary blood flow

1992 ◽  
Vol 262 (1) ◽  
pp. H68-H77
Author(s):  
F. L. Abel ◽  
R. R. Zhao ◽  
R. F. Bond
Keyword(s):  
Blood Flow ◽  
Coronary Blood Flow ◽  
Coronary Flow ◽  
Perfusion Pressure ◽  
Left Ventricular Pressure ◽  
Coronary Perfusion Pressure ◽  
Left Ventricular ◽  
Ventricular Pressure ◽  
Coronary Perfusion ◽  
Storage Site

Effects of ventricular compression on maximally dilated left circumflex coronary blood flow were investigated in seven mongrel dogs under pentobarbital anesthesia. The left circumflex artery was perfused with the animals' own blood at a constant pressure (63 mmHg) while left ventricular pressure was experimentally altered. Adenosine was infused to produce maximal vasodilation, verified by the hyperemic response to coronary occlusion. Alterations of peak left ventricular pressure from 50 to 250 mmHg resulted in a linear decrease in total circumflex flow of 1.10 ml.min-1 x 100 g heart wt-1 for each 10 mmHg of peak ventricular to coronary perfusion pressure gradient; a 2.6% decrease from control levels. Similar slopes were obtained for systolic and diastolic flows as for total mean flow, implying equal compressive forces in systole as in diastole. Increases in left ventricular end-diastolic pressure accounted for 29% of the flow changes associated with an increase in peak ventricular pressure. Doubling circumferential wall tension had a minimal effect on total circumflex flow. When the slopes were extrapolated to zero, assuming linearity, a peak left ventricular pressure of 385 mmHg greater than coronary perfusion pressure would be required to reduce coronary flow to zero. The experiments were repeated in five additional animals but at different perfusion pressures from 40 to 160 mmHg. Higher perfusion pressures gave similar results but with even less effect of ventricular pressure on coronary flow or coronary conductance. These results argue for an active storage site for systolic arterial flow in the dilated coronary system.

Composition and Mechanics of Routine Swimming of Rainbow Trout, Oncorhynchus mykiss

1991 ◽  
Vol 48 (4) ◽  
pp. 583-590 ◽  
Author(s):  
Paul W. Webb
Keyword(s):  
Rainbow Trout ◽  
Oncorhynchus Mykiss ◽  
Correction Factor ◽  
Swimming Speed ◽  
Angular Acceleration ◽  
Force Balance ◽  
Whole Body ◽  
Strongly Correlated ◽  
Rainbow Trout Oncorhynchus Mykiss ◽  
Tail Beat

Routine swimming encompasses all volitional motions of fish. It is usually assumed to be quasi-steady, i.e. routine swimming is mechanically equivalent to steady swimming. Routine swimming of rainbow trout, Oncorhynchus mykiss, was dominated by unsteady motions of linear and centripetal (angular) acceleration. Constant-speed swimming was rare. Mean speeds and acceleration rates were small. Tail-beat frequencies were nevertheless strongly correlated with mean swimming speed, but increased more rapidly with increasing speed in routine swimming than in steady swimming. Tail-beat amplitudes and propulsive wavelengths were similar to values seen in steady swimming. The composition of routine swimming and analysis of the force balance showed that routine swimming was not quasi-steady. Therefore, forces and rates of working should be estimated from a complete description of whole-body deformation. This is impractical. Drag dominated resistance in routine swimming, such that average thrust (= resistance) may be computed from mean speed and/or averaged kinematic variables for the trailing edge with a correction factor of approximately 3. Analysis of routine swimming may permit comparisons among a wider range of vertebrates than possible with commonly used methods.

How the efficiency of rainbow trout (Oncorhynchus mykiss) ventricular muscle changes with cycle frequency

2002 ◽  
Vol 205 (5) ◽  
pp. 697-706 ◽  
Author(s):  
Claire L. Harwood ◽  
Iain S. Young ◽  
John D. Altringham
Keyword(s):  
Heart Rate ◽  
Rainbow Trout ◽  
Oncorhynchus Mykiss ◽  
Cardiac Muscle ◽  
Power Output ◽  
Energy Cost ◽  
Total Efficiency ◽  
Ventricular Muscle ◽  
Cycle Frequency ◽  
Rainbow Trout Oncorhynchus Mykiss

SUMMARYDifferent species of animals require different cardiac performance and, in turn, their cardiac muscle exhibits different properties. A comparative approach can reveal a great deal about the mechanisms underlying myocardial contraction. Differences in myocardial Ca2+ handling between fish and mammals suggest a greater energy cost of activation in fish. Further, while there is considerable evidence that heart rate (or cycle frequency) should have a profound effect on the efficiency of teleost cardiac muscle, this effect has been largely overlooked. We set out to determine how cycle frequency affects the power output and efficiency of rainbow trout (Oncorhynchus mykiss) ventricular muscle and to relate this to the heart’s function in life. We measured power output and the rate of oxygen consumption (V̇O2) and then calculated efficiency over a physiologically realistic range of cycle frequencies.In contrast to mammalian cardiac muscle, in which V̇O2 increases with increasing heart rate, we found no significant change in V̇O2 in the teleost. However, power output increased by 25 % as cycle frequency was increased from 0.6 to 1.0 Hz, so net and total efficiency increased. A maximum total efficiency of 20 % was achieved at 0.8 Hz, whereas maximum power output occurred at 1.0 Hz. We propose that, since the heart operates continuously, high mechanical efficiency is a major adaptive advantage, particularly at lower heart rates corresponding to the more commonly used slower, sustainable swimming speeds. Efficiency was lower at the higher heart rates required during very fast swimming, which are used during escape or prey capture.If a fixed amount of Ca2+ is released and then resequestered each time the muscle is activated, the activation cost should increase with frequency. We had anticipated that this would have a large effect on the total energy cost of contraction. However, since V̇O2 remains constant, less oxygen is consumed per cycle at high frequencies. We suggest that a constant V̇O2 would be observed if the amount of activator Ca2+ were to decrease with frequency. This decrease in activation energy is consistent with the decrease in the systolic intracellular Ca2+ ([Ca2+]i) transient with increasing stimulation frequency seen in earlier studies.

Coronary hyperperfusion and myocardial metabolism in isolated and intact hearts

1987 ◽  
Vol 253 (5) ◽  
pp. H1271-H1278 ◽  
Author(s):  
W. P. Miller ◽  
N. Shimamoto ◽  
S. H. Nellis ◽  
A. J. Liedtke
Keyword(s):  
Blood Flow ◽  
Fatty Acid ◽  
Coronary Blood Flow ◽  
Myocardial Metabolism ◽  
Left Ventricular ◽  
Coronary Perfusion ◽  
Rat Hearts ◽  
Heart Preparation ◽  
Significant Change ◽  
Lv Volume

We determined the independent influence of coronary hyperperfusion on myocardial metabolism in isolated and intact hearts. In an isovolumic blood-perfused rat heart preparation working against a left ventricular (LV) balloon, the effect of increasing coronary perfusion pressure from 100 to 150 mmHg was assessed. In three groups of rat hearts LV volume was fixed to obtain LV peak pressures of 42 +/- 3, 101 +/- 5, and 130 +/- 6 mmHg. With coronary hyperperfusion, LV pressure increased 27, 18, and 16%, LV maximum time derivative of pressure (dP/dt) increased 39, 20, and 22%, and myocardial O2 consumption (VO2) increased 16, 17, and 33%, respectively. In a fourth group, LV peak pressure was held constant at 92 +/- 4 mmHg during coronary hyperperfusion by decreasing LV volume. In this group, despite an increase in coronary blood flow of 48%, there was no significant difference in LV maximum dP/dt or myocardial VO2. Thus, in isolated rat hearts, coronary hyperperfusion was not an independent stimulus to myocardial VO2. To further test this, the effect of coronary hyperperfusion on myocardial metabolism was studied in an intact working swine heart preparation where the cardiac output was fixed with a right heart bypass circuit. Fatty acid oxidation in the left anterior descending bed was assessed by production of 14CO2 from [14C(U)]palmitate. A comparison of coronary perfusion 106 +/- 5 vs. 197 +/- 5 mmHg resulted in no significant change in global LV function, including LV internal diameter. Despite a 70% increase in coronary blood flow, there was no significant change in myocardial VO2 or fatty acid utilization.(ABSTRACT TRUNCATED AT 250 WORDS)

Effects of gastric distension and feeding on cardiovascular variables in the shorthorn sculpin (Myoxocephalus scorpius)

2009 ◽  
Vol 296 (1) ◽  
pp. R171-R177 ◽  
Author(s):  
Henrik Seth ◽  
Michael Axelsson
Keyword(s):  
Rainbow Trout ◽  
Feeding Habits ◽  
Systemic Circulation ◽  
Gastric Distension ◽  
Subsequent Increase ◽  
Fish Meat ◽  
Rainbow Trout Oncorhynchus Mykiss ◽  
Chemically Induced ◽  
Aortic Blood Pressure ◽  
Myoxocephalus Scorpius

We have previously shown in rainbow trout ( Oncorhynchus mykiss) that gastric distension induces an instantaneous α-adrenoceptor-mediated increase in the dorsal aortic blood pressure (Pda), with no change in cardiac output (CO), gut blood flow (Qcma), or heart rate. To investigate if feeding habits affect these patterns and to compare the differences between gastric distension alone and feeding in the same experimental setting, we used the short-horn sculpin ( Myoxocephalus scorpius), an inactive ambush predator with a capacity to eat large meals. An inflatable balloon was placed in the stomach of one group while another group was fed fish meat. When distending the stomach with a volume corresponding to a meal of 8–10% body weight, there is a profound and long-lasting increase in systemic (123 ± 27%) and gastrointestinal (Rcma; 82 ± 24%) vascular resistance, leading to an increase in Pda (19%) without any change in CO or Qcma. After force-feeding, there is a rapid transient increase in Rcma (24 ± 4%) and an even larger Pda response (53%). There is also a subsequent increase in both CO (28 ± 8%) and Qcma (27 ± 9%) after 30 min. By 15 h, CO and Qcma increase further (41 ± 11 and 63 ± 14%, respectively), and this increase persists for up to 60 h. The increase in Qcma is mediated via both an increase in CO and a shunting of blood from the systemic circulation via a decrease in Rcma (34 ± 7%). In conclusion, the response to mechanical distension of the stomach is similar to what we have described in rainbow trout, and the postprandial gastrointestinal hyperemia is most likely chemically induced.

Alpha 2-adrenoceptor stimulation can augment coronary vasodilation maximally induced by adenosine in dogs

1989 ◽  
Vol 257 (1) ◽  
pp. H132-H140 ◽  
Author(s):  
M. Hori ◽  
M. Kitakaze ◽  
J. Tamai ◽  
K. Iwakura ◽  
A. Kitabatake ◽  
...  
Keyword(s):  
Blood Flow ◽  
Coronary Blood Flow ◽  
Small Dose ◽  
Reactive Hyperemia ◽  
Coronary Perfusion Pressure ◽  
Coronary Perfusion ◽  
Coronary Vasodilation ◽  
Beta Adrenoceptor ◽  
Adenosine Concentration ◽  
Hyperemic Flow

To determine whether alpha 2-adrenoceptor stimulation can augment adenosine-induced coronary vasodilation, 34 open-chest dogs were studied. When a small dose of clonidine (up to 0.24 micrograms.kg-1.min-1 ic) was administered under beta-adrenoceptor blockade, coronary blood flow [312 +/- 16 (SE) ml.100 g-1.min-1] maximally induced by intracoronary infusion of adenosine was further increased (P less than 0.05) by 66 +/- 16 ml.100 g-1.min-1, despite no significant changes in coronary perfusion pressure, myocardial oxygen consumption, and coronary venous adenosine concentration. However, when a larger dose of clonidine (0.36–0.60 micrograms.kg-1.min-1) was infused, adenosine-induced flow progressively decreased. This biphasic action of the alpha 2-adrenoceptor activity was also observed when the dose of norepinephrine was increased during alpha 1-adrenoceptor blockade with prazosin. Norepinephrine up to 0.24 micrograms.kg-1.min-1 (ic) further increased adenosine-induced coronary blood flow by 24 +/- 5% (P less than 0.001), whereas hyperemic flow was decreased by a larger dose of norepinephrine. In contrast to the alpha 2-adrenoceptor stimulation, the alpha 1-adrenoceptor stimulation (norepinephrine with yohimbine) progressively decreased coronary blood flow. Furthermore, with a small dose of clonidine, reactive hyperemic flow significantly increased compared with that without clonidine (303 +/- 13 vs. 355 +/- 13 ml.100 g-1.min-1, P less than 0.001), but a larger dose of clonidine adversely reduced reactive flow (254 +/- 18 ml.100 g-1.min-1, P less than 0.001). Adenosine release during reactive hyperemia with and without intracoronary infusions of clonidine were not altered significantly.(ABSTRACT TRUNCATED AT 250 WORDS)

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