scholarly journals Cardiac performance in the in situ perfused fish heart during extracellular acidosis: interactive effects of adrenaline

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.

1989 ◽  
Vol 67 (2) ◽  
pp. 274-280 ◽  
Author(s):  
A. P. Farrell ◽  
S. Small ◽  
M. S. Graham

While adrenergic stimulation and increased filling pressure of the heart are recognized to increase cardiac stroke volume in the trout heart, the effects of factors such as heart rate and oxygen supply have not been examined. The present study used isolated, saline-perfused trout hearts to determine the maximum cardiac performance during hypoxic perfusion and during changes in pacing frequency similar to the range of heart rate observed in intact trout. The threshold oxygen tension of the perfusate was between 25 and 46 Torr (3.33–6.13 kPa) for maintaining resting and maximum cardiac ouput, but was between 46 and 67 Torr (6.13 – 8.93 kPa) for maintaining maximum power output. Increasing the pacing frequency from 30 to 58 beats/min did not produce a proportionate increase in the maximum cardiac output because maximum stroke volume was reduced significantly. It is suggested that the reduction in maximum stroke volume occurs because atrial filling time is compromised at higher pacing frequencies in the isolated perfused heart.


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.


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.


2002 ◽  
Vol 205 (13) ◽  
pp. 1881-1888 ◽  
Author(s):  
Jason M. Blank ◽  
Jeffery M. Morrissette ◽  
Peter S. Davie ◽  
Barbara A. Block

SUMMARYTuna are endothermic fish with high metabolic rates, cardiac outputs and aerobic capacities. While tuna warm their skeletal muscle, viscera, brain and eyes, their hearts remain near ambient temperature, raising the possibility that cardiac performance may limit their thermal niches. We used an in situ perfused heart preparation to investigate the effects of acute temperature change and the effects of epinephrine and extracellular Ca2+ on cardiac function in yellowfin tuna (Thunnus albacares). Heart rate showed a strong temperature-dependence, ranging from 20 beats min-1 at 10 °C to 109 beats min-1 at 25 °C. Maximal stroke volume showed an inverse temperature-dependence,ranging from 1.4 ml kg-1 at 15 °C to 0.9 ml kg-1 at 25 °C. Maximal cardiac outputs were 27 ml kg-1 min-1at 10 °C and 98 ml kg-1 min-1 at 25 °C. There were no significant effects of perfusate epinephrine concentrations between 1 and 100 nmoll-1 at 20 °C. Increasing extracellular Ca2+ concentration from 1.84 to 7.36 mmoll-1 at 20°C produced significant increases in maximal stroke volume, cardiac output and myocardial power output. These data demonstrate that changes in heart rate and stroke volume are involved in maintaining cardiac output during temperature changes in tuna and support the hypothesis that cardiac performance may limit the thermal niches of yellowfin tuna.


1984 ◽  
Vol 62 (7) ◽  
pp. 1429-1435 ◽  
Author(s):  
A. P. Farrell ◽  
T. Hart ◽  
S. Wood ◽  
W. R. Driedzic

The effect of extracellular calcium ([Ca2+]e) on the performance of the in situ perfused sea raven heart was evaluated under nonacidotic, acidotic, and high work load conditions. Increases in [Ca2+]e improved power output of the nonacidotic heart and restored control levels of power output to the heart exposed to hypercapnic acidosis (1.8% CO2, pH 7.4). Extracellular acidosis severely curtailed the scope for cardiac work (increased cardiac output and afterload), and only a 50% increase in the control, nonacidotic power output was possible with increases in preload and saturating levels of [Formula: see text]. It is suggested that increases in preload are probably more important than increases in [Ca2+]e to improve cardiac performance in the seas raven heart during extracellular acidosis.


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.


1982 ◽  
Vol 60 (12) ◽  
pp. 3165-3171 ◽  
Author(s):  
A. P. Farrell ◽  
K. MacLeod ◽  
W. R. Driedzic

The preparation of the in situ heart was accomplished without any physical disturbance to the heart. The heart generated an intrinsic rhythm which was steady throughout the experiment and apparently was derived from the sinoatrial pacemaker. The power output developed by the in situ heart at physiological preloads and after loads was comparable to in vivo values. The effect of increasing preload (0 to 3 cmH2O) was a fourfold increase in stroke volume with little or no change in heart rate. When after load was changed (25 to 45 cmH2O) heart rate was unchanged and stroke volume was usually maintained. As a consequence, cardiac output was maintained by intrinsic factors alone at a higher work load. Epinephrine (10−9 to 10−5 M) in the perfusate produced relatively weak positive chronotropic and inotropic effects. The increase in cardiac output produced by epinephrine was small compared with the intrinsic changes evoked when preload was raised.


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