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

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.

1995 ◽  
Vol 269 (5) ◽  
pp. R1258-R1266 ◽  
Author(s):  
A. K. Gamperl ◽  
M. Axelsson ◽  
A. P. Farrell

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.


2019 ◽  
Vol 7 (1) ◽  
Author(s):  
Stuart Egginton ◽  
Michael Axelsson ◽  
Elizabeth L Crockett ◽  
Kristin M O’Brien ◽  
Anthony P Farrell

Abstract Antarctic notothenioids, some of which lack myoglobin (Mb) and/or haemoglobin (Hb), are considered extremely stenothermal, which raises conservation concerns since Polar regions are warming at unprecedented rates. Without reliable estimates of maximum cardiac output ($\dot{Q}$), it is impossible to assess their physiological scope in response to warming seas. Therefore, we compared cardiac performance of two icefish species, Chionodraco rastrospinosus (Hb−Mb+) and Chaenocephalus aceratus (Hb−Mb−), with a related notothenioid, Notothenia coriiceps (Hb+Mb+) using an in situ perfused heart preparation. The maximum $\dot{Q}$, heart rate (fH), maximum cardiac work (WC) and relative ventricular mass of N. coriiceps at 1°C were comparable to temperate-water teleosts, and acute warming to 4°C increased fH and WC, as expected. In contrast, icefish hearts accommodated a higher maximum stroke volume (VS) and maximum $\dot{Q}$ at 1°C, but their unusually large hearts had a lower fH and maximum afterload tolerance than N. coriiceps at 1°C. Furthermore, maximum VS, maximum $\dot{Q}$ and fH were all significantly higher for the Hb−Mb+ condition compared with the Hb−Mb− condition, a potential selective advantage when coping with environmental warming. Like N. coriiceps, both icefish species increased fH at 4°C. Acutely warming C. aceratus increased maximum $\dot{Q}$, while C. rastrospinosus (like N. coriiceps) held at 4°C for 1 week maintained maximum $\dot{Q}$ when tested at 4°C. These experiments involving short-term warming should be followed up with long-term acclimation studies, since the maximum cardiac performance of these three Antarctic species studied seem to be tolerant of temperatures in excess of predictions associated with global warming.


1992 ◽  
Vol 263 (4) ◽  
pp. R798-R804 ◽  
Author(s):  
P. G. Arthur ◽  
J. E. Keen ◽  
P. W. Hochachka ◽  
A. P. Farrell

An in situ perfused heart preparation was used to study the effects of severe hypoxia in the rainbow trout, Oncorhynchus mykiss. Hypoxic trout hearts were capable of generating similar power outputs and ATP turnovers to normoxic counterparts at subphysiological work regimes. However, lactate efflux was 35-fold higher and glycolytic rate was calculated to be > 10-fold higher in hypoxic than in normoxic hearts. The surprising ability of trout hearts to withstand severe hypoxia appears to be related to the rapid removal of lactate and associated protons from the heart. An increase in power demand to normal in vivo levels caused rapid failure in hypoxic hearts. Failure was caused by a decline in stroke volume (contractility) and was not a consequence of heart rate deterioration. Hypoxia caused marked declines in the concentration of creatine phosphate but not ATP, and we suggest that an increase in intracellular phosphate was the primary cause of failure.


1991 ◽  
Vol 69 (7) ◽  
pp. 1822-1828 ◽  
Author(s):  
Peter S. Davie ◽  
Anthony P. Farrell

An isolated preparation of the heart of the spiny dogfish, Squalus acanthias, was developed that allowed control of filling and output pressures and perfusion of the coronary arteries. Cardiac output and stroke volume, but not frequency, were dependent upon atrial filling pressure. The mean maximum cardiac power output of 1.76 mW/g ventricle mass was achieved at high stroke volumes and moderate output pressures (29 cmH2O). When stroke volume was set at half of its measured maximum, increases in output pressure did not affect stroke volume up to pressures near 46 cmH2O, at which point cardiac power output was 1.4 mW/g ventricle mass. In the absence of coronary perfusion, hypoxic perfusion of the heart lumen reduced maximum power output by 38% at 58 ± 3.4 torr and by 64% at 7.7 ± 0.8 torr. Perfusion of the coronary circulation with air-saturated saline or red cell suspensions had no effect on hearts pumping air-saturated saline or hypoxic [Formula: see text] saline, but significantly increased the maximum power output of the hearts pumping severely hypoxic [Formula: see text] saline.


1993 ◽  
Vol 71 (12) ◽  
pp. 946-951 ◽  
Author(s):  
H. Amory ◽  
K. McEntee ◽  
A. S. Linden ◽  
D. J. M. Desmecht ◽  
J. M. L. Beduin ◽  
...  

Hereditary muscular hypertrophy is a character that has been selected in several animal species for industrial meat production. The selection of this character in cattle produces animals of exceptional commercial value but ones with a lower aerobic capacity than that of conventional cattle. The purpose of this work was to study the role of cardiac function as a potential limiting factor of aerobic capacity in double-muscled calves. Two groups of healthy calves were studied, one consisting of nine calves of conventional conformation and the other of nine double-muscled calves. Pulmonary arterial and capillary wedge, central venous, and systemic arterial pressures were measured by fluid-filled catheters and recorded together with the electrocardiogram. Cardiac output was measured by the thermodilution technique. From these measurements, the heart rate, the cardiac and the stroke indices, the pulmonary and the systemic vascular resistances, and the cardiac power output were calculated. The parameters were recorded under basal resting conditions and during incremental dobutamine challenge, which allowed determination of the resting cardiac power output, the cardiac pumping capability, and the cardiac reserve. Dobutamine challenge induced a significant rise in cardiac and stroke indices, heart rate, and cardiac power output, a significant decrease in pulmonary and systemic vascular resistances, and no change in systemic and pulmonary arterial pressures. The cardiac reserve obtained in the present study was low in comparison with those previously reported in humans, dogs, and horses. This may be related to the poor running capability of bovine species relative to that of the former species. The double-muscled calves had significantly lower cardiac and stroke indices, resting cardiac power output, cardiac pumping capability, and cardiac reserve than did conventional calves. Therefore, the cardiac performance, capability, and reserve were reduced in double-muscled calves. It was concluded that cardiac performance is a critical step in the oxygen-transport pathway in double-muscled cattle.Key words: cattle, hereditary muscular hypertrophy, oxygen consumption, cardiovascular system, cardiac power output.


1983 ◽  
Vol 107 (1) ◽  
pp. 415-429 ◽  
Author(s):  
A. P. Farrell ◽  
K. R. MacLeod ◽  
W. R. Driedzic ◽  
S. Wood

The physiological integrity of the in situ perfused heart of the ocean pout was established by its ability to maintain cardiac output (Q) over a range of work loads, and by the dependence of Q upon the filling pressure of the heart. Similar observations have been reported previously for the in situ perfused heart of the sea raven. Physiological levels of extracellular acidosis (pH 7.6/1% CO2 and pH 7.4/2% CO2) significantly depressed cardiac performance in sea raven and ocean pout hearts in situ. Negative chronotropic and inotropic responses were observed. Adrenaline (AD; 10(−7) M) under control conditions (pH 7.9/0.5% CO2) produced a sustained tachycardia. The tachycardia reduced filling time of the ventricle and stroke volume was compromised because of the constant preload to the heart. Consequently, AD produced only an initial, transient increase in stroke volume and Q. Thereafter, stroke volume was reduced in proportion with the increase in heart rate, and Q remained unchanged. The combined challenge of extracellular acidosis and AD demonstrated interactive effects between AD and acidosis in situ. Q and power output were maintained in both species at both levels of extracellular acidosis during the combined challenge. Thus AD alone can maintain (but not improve upon) basal Q during extracellular acidosis. The effects of extracellular acidosis, circulating catecholamines and venous return pressure to the heart are discussed in relation to the regulation of Q following exhaustive exercise.


1994 ◽  
Vol 186 (1) ◽  
pp. 269-288 ◽  
Author(s):  
C. Franklin ◽  
M. Axelsson

An in situ perfused crocodile (Crocodylus porosus) heart preparation was developed to investigate the effects of input and output pressure on cardiac dynamics and to determine the conditions that lead to a right-to-left cardiac shunt. The pericardium was kept intact, both the left and right atria were perfused and all three outflow tracts (right aortic, left aortic and pulmonary) were cannulated, enabling pressures and flows to be monitored. The perfused heart preparation had an intrinsic heart rate of 34 beats min-1 and generated a physiological power output. Both the left and right sides of the heart were sensitive to filling pressure. Increasing the filling pressure to both atria resulted in an increase in stroke volume and cardiac output (Frank­Starling effect). Increasing the filling pressure to the right atrium also had a positive chronotropic effect. Large right ventricular stroke volumes initiated a right-to-left shunt, despite the left aorta having a pressure 1.5 kPa higher than the pulmonary output pressure. The left ventricle was able to maintain its output and stroke volume up to an output pressure of approximately 8 kPa. However, the right ventricle was significantly weaker. Right ventricular output and stroke volume showed a marked decrease when the output pressure was increased above 5 kPa. A right-to-left shunt occurred when pulmonary output pressure was increased. Surprisingly, a shunt occurred into the left aorta before the pressure in the pulmonary artery became greater than that in the left aorta. Once the pressure in the pulmonary artery exceeded the left aortic pressure, pulmonary artery flow ceased and right ventricular output was solely via the left aorta. A right-to-left shunt could also be initiated by increasing the filling pressure to the left atrium.


1994 ◽  
Vol 191 (1) ◽  
pp. 207-229 ◽  
Author(s):  
A Farrell ◽  
C Franklin ◽  
P Arthur ◽  
H Thorarensen ◽  
K Cousins

We developed an in situ perfused turtle (Chrysemys scripta) heart preparation to study its intrinsic mechanical properties at 5°C and 15°C using normoxic and anoxic perfusion conditions. The in situ preparation proved durable and stable. At 15°C and a spontaneous heart rate of 23.4 beats min-1, maximum stroke volume was 2.54 ml kg-1 body mass, maximum cardiac output was 62.5 ml min-1 kg-1 and maximum cardiac myocardial power output was 1.50 mW g-1 ventricular mass. There was good agreement between these values and those previously obtained in vivo. Furthermore, since the maximum stroke volume observed here was numerically equivalent to that observed in ventilating C. scripta in vivo, it seems likely that C. scripta has little scope to increase stroke volume to a level much beyond that observed in the resting animal through intrinsic mechanisms alone. The ability of the perfused turtle heart to maintain stroke volume when diastolic afterload was raised (homeometric regulation) was relatively poor. At 5°C, the spontaneous heart rate (8.1 beats min-1) was threefold lower and homeometric regulation was impaired, but maximum stroke volume (2.25 ml kg-1) was not significantly reduced compared with the value at 15°C. The significantly lower maximum values for cardiac output (18.9 ml min-1 kg-1) and power output (0.39 mW g-1 ventricular mass) at 5°C were largely related to pronounced negative chronotropy with only a relatively small negative inotropy. Anoxia had weak negative chronotropic effects and marked negative inotropic effects at both temperatures. Negative inotropy affected pressure development to a greater degree than maximum flow and this difference was more pronounced at 5°C than at 15°C. The maximum anoxic cardiac power output value at 15°C (0.77 mW g-1 ventricular mass) was not that different from values previously obtained for the performance of anoxic rainbow trout and hagfish hearts. In view of this, we conclude that the ability of turtles to overwinter under anoxic conditions depends more on their ability to reduce cardiac work to a level that can be supported through glycolysis than on their cardiac glycolytic potential being exceptional.


1996 ◽  
Vol 199 (3) ◽  
pp. 663-672 ◽  
Author(s):  
A Farrell ◽  
A Gamperl ◽  
J Hicks ◽  
H Shiels ◽  
K Jain

Numerous studies have examined the effect of temperature on in vivo and in situ cardiovascular function in trout. However, little information exists on cardiac function at temperatures near the trout's upper lethal limit. This study measured routine and maximum in situ cardiac performance in rainbow trout (Oncorhynchus mykiss) following acclimation to 15, 18 and 22 °C, under conditions of tonic (30 nmol l-1), intermediate (60 nmol l-1) and maximal (200 nmol l-1) adrenergic stimulation. Heart rate increased significantly with both temperature and adrenaline concentration. The Q10 values for heart rate ranged from 1.28 at 30 nmol l-1 adrenaline to 1.36 at 200 nmol l-1 adrenaline. In contrast to heart rate, maximum stroke volume declined by approximately 20 % (from 1.0 to 0.8 ml kg-1) as temperature increased from 15 to 22 °C. This decrease was not alleviated by maximally stimulating the heart with 200 nmol l-1 adrenaline. Because of the equal and opposite effects of increasing temperature on heart rate and stroke volume, maximum cardiac output did not increase between 15 and 22 °C. Maximum power output decreased (by approximately 10-15 %) at all adrenaline concentrations as temperature increased. This reduction reflected a poorer pressure-generating ability at temperatures above 15 °C. These results, in combination with earlier work, suggest (1) that peak cardiac performance occurs around the trout's preferred temperature and well below its upper lethal limit; (2) that the diminished cardiac function concomitant with acclimation to high temperatures was associated with inotropic failure; (3) that Q10 values for cardiac rate functions, other than heart rate per se, have a limited predictive value at temperatures above the trout's preferred temperature; and (4) that heart rate is a poor indicator of cardiac function at temperatures above 15 °C.


1985 ◽  
Vol 118 (1) ◽  
pp. 173-183 ◽  
Author(s):  
MARK GRAHAM ◽  
ANTHONY FARRELL

1. An in situ heart preparation was used to evaluate cardiac performance in the sea raven, Hemitripterus americanus, under physiological inflow and outflow pressure conditions. Winter and summer fish were subjected to an acute 10°C temperature change from the seasonal ambient value. The maximum cardiac output (V·b) under each temperature condition was determined by altering inflow pressure to the heart. 2. Acute temperature increase produced positive chronotropic and inotropic effects in winter fish. Acute temperature decrease produced a negative chronotropic and inotropic effect in summer fish. 3. The inotropic and chronotropic states of the heart were different in winter and summer fish. Intrinsic heart rate was higher in summer fish at all experimental temperatures. The sensitivity of the summer fish hearts to input pressure was also greater, especially during the warm experimental temperatures. 4. It was evident from heartbeat rate measurements and power output calculations that the advent of summer and winter seasons did not promote any compensatory ability in intrinsic heart function.


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