The Effect of Body Mass and Temperature on the Heart Rate, Stroke Volume, and Cardiac Output of Larvae of the Rainbow Trout,Oncorhynchus mykiss

1998 ◽  
Vol 71 (2) ◽  
pp. 191-197 ◽  
Author(s):  
Tatjana Mirkovic ◽  
Peter Rombough
Keyword(s):  
Heart Rate ◽  
Cardiac Output ◽  
Rainbow Trout ◽  
Stroke Volume ◽  
Oncorhynchus Mykiss ◽  
Body Mass ◽  
Rainbow Trout Oncorhynchus Mykiss

Adrenergic control of venous capacitance during moderate hypoxia in the rainbow trout (Oncorhynchus mykiss): role of neural and circulating catecholamines

2006 ◽  
Vol 291 (3) ◽  
pp. R711-R718 ◽  
Author(s):  
Erik Sandblom ◽  
Michael Axelsson
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Cardiac Output ◽  
Rainbow Trout ◽  
Oncorhynchus Mykiss ◽  
Blood Volume ◽  
Body Mass ◽  
Venous Capacitance ◽  
Moderate Hypoxia ◽  
Rainbow Trout Oncorhynchus Mykiss

Central venous blood pressure (Pven) increases in response to hypoxia in rainbow trout ( Oncorhynchus mykiss), but details on the control mechanisms of the venous vasculature during hypoxia have not been studied in fish. Basic cardiovascular variables including Pven, dorsal aortic blood pressure, cardiac output, and heart rate were monitored in vivo during normoxia and moderate hypoxia (PWO2 = ∼9 kPa), where PWO2 is water oxygen partial pressure. Venous capacitance curves for normoxia and hypoxia were constructed at 80–100, 90–110, and 100–120% of total blood volume by transiently (8 s) occluding the ventral aorta and measure Pven during circulatory arrest to estimate the mean circulatory filling pressure (MCFP). This allowed for estimates of hypoxia-induced changes in unstressed blood volume (USBV) and venous compliance. MCFP increased due to a decreased USBV at all blood volumes during hypoxia. These venous responses were blocked by α-adrenoceptor blockade with prazosin (1 mg/kg body mass). MCFP still increased during hypoxia after pretreatment with the adrenergic nerve-blocking agent bretylium (10 mg/kg body mass), but the decrease in USBV only persisted at 80–100% blood volume, whereas vascular capacitance decreased significantly at 90–110% blood volume. In all treatments, hypoxia typically reduced heart rate while cardiac output was maintained through a compensatory increase in stroke volume. Despite the markedly reduced response in venous capacitance after adrenergic blockade, Pven always increased in response to hypoxia. This study reveals that venous capacitance in rainbow trout is actively modulated in response to hypoxia by an α-adrenergic mechanism with both humoral and neural components.

Cardiovascular changes in the exercising emu

1983 ◽  
Vol 104 (1) ◽  
pp. 193-201 ◽  
Author(s):  
B. Grubb ◽  
D. D. Jorgensen ◽  
M. Conner
Keyword(s):  
Heart Rate ◽  
Cardiac Output ◽  
Oxygen Consumption ◽  
Stroke Volume ◽  
Oxygen Content ◽  
Body Mass ◽  
Fold Increase ◽  
Exercise Heart Rate ◽  
Rate Of Oxygen Consumption ◽  
Cardiovascular Variables

Cardiovascular variables were studied as a function of oxygen consumption in the emu, a large, flightless ratite bird well suited to treadmill exercise. At the highest level of exercise, the birds' rate of oxygen consumption (VO2) was approximately 11.4 times the resting level (4.2 ml kg-1 min-1). Cardiac output was linearly related to VO2, increasing 9.5 ml for each 1 ml increase in oxygen consumption. The increase in cardiac output is similar to that in other birds, but appears to be larger than in mammals. The venous oxygen content dropped during exercise, thus increasing the arteriovenous oxygen content difference. At the highest levels of exercise, heart rate showed a 3.9-fold increase over the resting rate (45.8 beats min-1). The mean resting specific stroke volume was 1.5 ml per kg body mass, which is larger than shown by most mammals. However, birds have larger hearts relative to body mass than do mammals, and stroke volume expressed per gram of heart (0.18 ml g-1) is similar to that for mammals. Stroke volume showed a 1.8-fold increase as a result of exercise in the emus, but a change in heart rate plays a greater role in increasing cardiac output during exercise.

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.

scholarly journals Temperature-dependent development of cardiac activity in unrestrained larvae of the minnow Phoxinus phoxinus

2000 ◽  
Vol 279 (5) ◽  
pp. R1634-R1640 ◽  
Author(s):  
G. Schönweger ◽  
T. Schwerte ◽  
B. Pelster
Keyword(s):  
Heart Rate ◽  
Cardiac Output ◽  
Stroke Volume ◽  
Incubation Period ◽  
Body Mass ◽  
Metabolic Activity ◽  
Cardiac Activity ◽  
Swim Bladder ◽  
Phoxinus Phoxinus ◽  
Swim Bladder Inflation

The minnow ( Phoxinus phoxinus) was raised up to the stage of swim bladder inflation at temperatures between 10°C and 25°C, and the time of development significantly decreased at higher temperatures. Accordingly, initiation of cardiac activity was observed at day 2 in 25°C animals and at day 4 in 12.5°C animals. Only a minor increase in body mass was observed during the incubation period, and, at the end of the incubation period, animals raised at 25°C did not have a significantly lower body mass compared with animals raised at 15°C. Metabolic activity, determined as the rate of oxygen consumption of a larva, increased from 3.3 to 19.5 nmol/h during development at 15°C and from 5.6 to 47.6 nmol/h during development at 25°C. Heart rate showed a clear correlation to developmental stage as well as to developmental temperature, but at the onset of cardiac activity, diastolic ventricular volume and also stroke volume were higher at the lower temperatures. Furthermore, stroke volume increased with development, except for the group incubated at 12.5°C, in which stroke volume decreased with development. Initial cardiac output showed no correlation to incubation temperature. Although metabolic activity increased severalfold during development from egg to the stage of swim bladder inflation at 15°C and at 25°C, weight-specific cardiac output increased only by ∼40% with proceeding development. At 12.5°C, cardiac output remained almost constant until opening of the swim bladder. The data support the notion that oxygen transport is not the major function of the circulatory system at this stage of development. The changes in heart rate with temperature appear to be due to the intrinsic properties of the pacemaker; there was no indication for a regulated response.

Cholecystokinin as a regulator of cardiac function and postprandial gastrointestinal blood flow in rainbow trout (Oncorhynchus mykiss)

2010 ◽  
Vol 298 (5) ◽  
pp. R1240-R1248 ◽  
Author(s):  
Henrik Seth ◽  
Albin Gräns ◽  
Michael Axelsson
Keyword(s):  
Blood Flow ◽  
Cardiac Output ◽  
Rainbow Trout ◽  
Oncorhynchus Mykiss ◽  
Direct Effect ◽  
Flow Profile ◽  
Subsequent Increase ◽  
Physiological Concentration ◽  
Rainbow Trout Oncorhynchus Mykiss ◽  
Gastrointestinal Blood Flow

We have studied the potential role of CCK as a regulator/modulator of the postprandial increase in gastrointestinal blood flow. Rainbow trout ( Oncorhynchus mykiss ) were instrumented with pulsed Doppler flow probes to measure the effects of CCK on cardiac output and gastrointestinal blood flow. Furthermore, vascular preparations were used to study the direct effects of CCK on the vessels. In addition, we used in situ perfused hearts to further study the effects of CCK on the cardiovascular system. When the sulfated form of CCK-8 was injected at a physiological concentration (0.19 pmol/kg) in vivo, there was a significant increase in the gastrointestinal blood flow (18 ± 4%). This increase in gastrointestinal blood flow was followed by a subsequent increase in cardiac output (30 ± 6%). When the dose was increased to 0.76 pmol/kg, there was only a 14 ± 6% increase in gastrointestinal blood flow; possibly due to a dose-dependent increase in the gill vascular resistance as previously reported or a direct effect on the heart. Nevertheless, CCK did not affect the isolated vessel preparations, and thus, it seems unlikely that CCK has a direct effect on the blood vessels of the second or third order. CCK did, however, have profound effects on the dynamics of the heart, and without a change in cardiac output, there was a significant increase in the amplitude (59 ± 4%) and rate (dQ/d t: 55 ± 4%; -dQ/d t: 208 ± 49%) of the phasic flow profile. If and how this might be coupled to a postprandial gastrointestinal hyperemia remains to be determined. We conclude that CCK has the potential as a regulator of the postprandial gastrointestinal blood flow in fish and most likely has its effect by inducing a gastrointestinal hyperemia. The mechanism by which CCK acts is at present unknown.

Maximum cardiac performance of rainbow trout (Oncorhynchus mykiss) at temperatures approaching their upper lethal limit

1996 ◽  
Vol 199 (3) ◽  
pp. 663-672 ◽  
Author(s):  
A Farrell ◽  
A Gamperl ◽  
J Hicks ◽  
H Shiels ◽  
K Jain
Keyword(s):  
Heart Rate ◽  
Rainbow Trout ◽  
Stroke Volume ◽  
Cardiac Function ◽  
Cardiac Performance ◽  
Preferred Temperature ◽  
Rainbow Trout Oncorhynchus Mykiss ◽  
Lethal Limit ◽  
Q10 Values

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.

Influence of cycle frequency, muscle strain and muscle length on work and power production of rainbow trout (Oncorhynchus mykiss) ventricular muscle

1998 ◽  
Vol 201 (19) ◽  
pp. 2723-2733 ◽  
Author(s):  
CL Harwood ◽  
IS Young ◽  
JD Altringham
Keyword(s):  
Rainbow Trout ◽  
Stroke Volume ◽  
Oncorhynchus Mykiss ◽  
Power Output ◽  
Muscle Length ◽  
Maximum Power ◽  
Muscle Strain ◽  
Cycle Frequency ◽  
Rainbow Trout Oncorhynchus Mykiss ◽  
Maximum Work

This study investigates the effects of cycle frequency, strain and length on work and power output of isolated rainbow trout (Oncorhynchus mykiss) ventricular preparations using the work loop technique. These effects are discussed in the context of the whole heart using analogies with heart rate, stroke volume and end-diastolic volume. Power output was dependent on cycle frequency, increasing threefold beween 0.3 and 1.1 Hz. The frequency for maximum power output was approximately 1.1 Hz, corresponding to the frequency for maximum power in perfused heart experiments. The length for maximum work production (Lopt) was found to be the same as the length for maximum isometric force production (Lmax). The decline in net work at lengths greater than Lopt/Lmax was attributed to an increase in passive work (the work done on an unstimulated muscle) or to hysteresis and to a large increase in lengthening work. The strain yielding maximum work decreased with increasing frequency. This is discussed in the context of the decline in stroke volume observed at increased heart rates in vivo. Muscle strain in intact hearts paced at 0.3 Hz was +/-11.9 % (23.8 % peak to peak), a value similar to the optimum strain at 0.3 Hz in vitro (+/-12 %).

Venous hemodynamic responses to acute temperature increase in the rainbow trout (Oncorhynchus mykiss)

2007 ◽  
Vol 292 (6) ◽  
pp. R2292-R2298 ◽  
Author(s):  
Erik Sandblom ◽  
Michael Axelsson
Keyword(s):  
Cardiac Output ◽  
Rainbow Trout ◽  
Oncorhynchus Mykiss ◽  
Temperature Increase ◽  
Venous Return ◽  
Filling Pressure ◽  
Venous Capacitance ◽  
Cardiac Filling Pressure ◽  
Rainbow Trout Oncorhynchus Mykiss ◽  
Cardiac Filling

Many ectotherms regularly experience considerable short-term variations in environmental temperature, which affects their body temperature. Here we investigate the cardiovascular responses to a stepwise acute temperature increase from 10 to 13 and 16°C in rainbow trout ( Oncorhynchus mykiss). Cardiac output increased by 20 and 31% at 13 and 16°C, respectively. This increase was entirely mediated by an increased heart rate (fH), whereas stroke volume (SV) decreased significantly by 20% at 16°C. The mean circulatory filling pressure (MCFP), a measure of venous capacitance, increased with temperature. Central venous pressure (Pven) did not change, whereas the pressure gradient for venous return (MCFP-Pven) was significantly increased at both 13 and 16°C. Blood volume, as measured by the dilution of 51Cr-labeled red blood cells, was temperature insensitive in both intact and splenectomized trout. This study demonstrates that venous capacitance in trout decreases, but cardiac filling pressure as estimated by Pven does not change when cardiac output increases during an acute temperature increase. SV was compromised as fH increased with temperature. The decreased capacitance likely serves to prevent passive pooling of blood in the venous periphery and to maintain cardiac filling pressure and a favorable pressure gradient for venous return.

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