Non-invasive quantification of cardiac stroke volume in the edible crab Cancer pagurus

Abstract Background Brachyuran crabs can effectively modulate cardiac stroke volume independently of heart rate in response to abiotic drivers. Non-invasive techniques can help to improve the understanding of cardiac performance parameters of these animals. This study demonstrates the in vivo quantification of cardiac performance parameters through magnetic resonance imaging (MRI) on the edible crab Cancer pagurus. Furthermore, the suitability of signal integrals of infra-red photoplethysmographs as a qualitative tool is assessed under severe hypoxia. Results Multi-slice self-gated cardiac cinematic (CINE) MRI revealed the structure and motion of the ventricle to quantify heart rates, end-diastolic volume, end-systolic volume, stroke volume and ejection fraction. CINE MRI showed that stroke volumes increased under hypoxia because of a reduction of end-systolic volumes at constant end-diastolic volumes. Plethysmograph recordings allowed for automated heart rate measurements but determination of a qualitative stroke volume proxy strongly depended on the position of the sensor on the animal. Both techniques revealed a doubling in stroke volumes after 6 h under severe hypoxia (water PO2 = 15% air saturation). Conclusions MRI has allowed for detailed descriptions of cardiac performance in intact animals under hypoxia. The temporal resolution of quantitative non-invasive CINE MRI is limited but should encourage further refining. The stroke volume proxy based on plethysmograph recordings is feasible to complement other cardiac measurements over time. The presented methods allow for non-destructive in vivo determinations of multiple cardiac performance parameters, with the possibility to study neuro-hormonal or environmental effects on decapod cardio physiology.

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Effect of heart rate and hypoxia on the performance of a perfused trout heart

Canadian Journal of Zoology ◽

10.1139/z89-040 ◽

1989 ◽

Vol 67 (2) ◽

pp. 274-280 ◽

Cited By ~ 28

Author(s):

A. P. Farrell ◽

S. Small ◽

M. S. Graham

Keyword(s):

Heart Rate ◽

Stroke Volume ◽

Oxygen Supply ◽

Filling Pressure ◽

Cardiac Performance ◽

Isolated Perfused Heart ◽

Adrenergic Stimulation ◽

Perfused Heart ◽

Filling Time ◽

Cardiac Stroke Volume

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.

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Interaction of interval-force relationship with aortic pressure and stroke volume

American Journal of Physiology-Legacy Content ◽

10.1152/ajplegacy.1976.230.4.893 ◽

1976 ◽

Vol 230 (4) ◽

pp. 893-900 ◽

Cited By ~ 2

Author(s):

ER Powers ◽

Foster ◽

Powell WJ

Keyword(s):

Heart Rate ◽

Stroke Volume ◽

Diastolic Pressure ◽

Aortic Pressure ◽

Left Ventricular ◽

Cardiac Performance ◽

Right Heart ◽

Anesthetized Dogs ◽

Right Heart Bypass ◽

Force Relationship

The modification by aortic pressure and stroke volume of the response in cardiac performance to increases in heart rate (interval-force relationship) has not been previously studied. To investigate this interaction, 30 adrenergically blocked anesthetized dogs on right heart bypass were studied. At constant low aortic pressure and stroke volume, increasing heart rate (over the entire range 60-180) is associated with a continuously increasing stroke power, decreasing systolic ejection period, and an unchanging left ventricular end-diastolic pressure and circumference. At increased aortic pressure or stroke volume at low rates (60-120), increases in heart rate were associated with an increased performance. However, at increased aortic pressure or stroke volume at high rates (120-180), increases in heart rate were associated with a leveling or decrease in performance. Thus, an increase in aortic pressure or stroke volume results in an accentuation of the improvement in cardiac performance observed with increases in heart rate, but this response is limited to a low heart rate range. Therefore, the hemodynamic response to given increases in heart rate is critically dependent on aortic pressure and stroke volume.

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Crustacean cardioexcitatory peptides may inhibit the heart in vivo.

Journal of Experimental Biology ◽

10.1242/jeb.198.12.2547 ◽

1995 ◽

Vol 198 (12) ◽

pp. 2547-2550 ◽

Cited By ~ 3

Author(s):

I J McGaw ◽

J L Wilkens ◽

B R McMahon ◽

C N Airriess

Keyword(s):

Stroke Volume ◽

Isolated Heart ◽

Cancer Magister ◽

Isolated Hearts ◽

Cardiovascular Performance ◽

Cast Doubt ◽

Cardiac Stroke Volume

Peptide neurohormones exist as functionally similar analogues in a wide variety of invertebrate and vertebrate phyla, and many have been implicated as cardiovascular regulators. In decapod crustaceans, these include the pentapeptide proctolin, crustacean cardioactive peptide (CCAP) and the FMRF amide-related peptides F1 and F2, all of which are found in the pericardial organs located immediately upstream of the heart. Cardioexcitatory activity has been demonstrated by these four peptides in both isolated and semi-isolated arthropod hearts; CCAP, however, has minimal effects on the heart of Cancer magister. In the present study, we determined the effects of proctolin, F1 and F2 on the heart of the crab C. magister in both in vitro (semi-isolated heart) and in vivo (whole animal) preparations. In semi-isolated hearts, infusion of each peptide caused cardioexcitation, increasing the rate and stroke volume of the heart. In whole crabs, the peptides were cardioinhibitory; the strongest effects were observed with F1 and F2, which dramatically decreased heart rate, cardiac stroke volume and cardiac output. These results cast doubt on current perceptions of the functional role of cardioactive peptides in the regulation of invertebrate cardiovascular performance in vivo.

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Cardiac-generated sympathetic stress alters heart-brain communication, reduces EEG-theta activity, and increases locomotor behavior

10.1101/2021.07.19.452502 ◽

2021 ◽

Author(s):

Jacopo Agrimi ◽

Danilo Menicucci ◽

Marco Laurino ◽

Chelsea Mackey ◽

Laila Hasnain ◽

...

Keyword(s):

Heart Rate ◽

Heart Rhythm ◽

Simultaneous Recording ◽

Cardiac Performance ◽

Autonomic Control ◽

Theta Activity ◽

Movement Speed ◽

Brain Functions ◽

Sympathetic Stress

Brain modulation of myocardial activity via the autonomic nervous system is increasingly well characterized. Conversely, how primary alterations in cardiac function, such as an intrinsic increase in heart rate or contractility, reverberate on brain signaling/adaptive behaviors - in a bottom-up modality - remains largely unclear. Mice with cardiac-selective overexpression of adenylyl cyclase type 8 (TGAC8) display increased heart rate and reduced heart rhythm complexity associated with a nearly abolished response to external sympathetic inputs. Here, we tested whether chronically elevated intrinsic cardiac performance alters the heart-brain informational flow, affecting brain signaling and, thus, behavior. To this end, we employed dual lead telemetry for simultaneous recording of EEG and EKG time series in awake, freely behaving TGAC8 mice and wild-type (WT) littermates. We recorded EEG and EKG signals, while monitoring mouse behavior with established tests. Using heart rate variability (HRV) in vivo and isolated atria response to sympathomimetic agents, we first confirmed that the TGAC8 murine heart evades autonomic control. The EEG analysis revealed a substantial drop in theta-2 (4-7 Hz) activity in these transgenic mice. Next, we traced the informational flow between EKG and EEG in the theta-2 frequency band via the Granger causality statistical approach and we found a substantial decrement in the extent of heart/brain bidirectional communication. Finally, TGAC8 mice displayed heightened locomotor activity in terms of behavior, with higher total time mobile, distance traveled, and movement speed while freezing behavior was reduced. Increased locomotion correlated negatively with theta-2 waves count and amplitude. Our study shows that cardiac-born persistent sympathetic stress disrupts the information flow between the heart and brain while influencing central physiological patterns, such as theta activity that controls locomotion. Thus, cardiac-initiated disorders, such as persistently elevated cardiac performance that escapes autonomic control, are penetrant enough to alter brain functions and, thus, primary adaptive behavioral responses.

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Cardiac stroke volume predicts progressive central hypovolemia by three different non‐invasive methods

The FASEB Journal ◽

10.1096/fasebj.27.1_supplement.1193.1 ◽

2013 ◽

Vol 27 (S1) ◽

Author(s):

Nathalie Linn Anikken Holme ◽

Erling Bekkestad Rein ◽

Lars Walløe ◽

Marianne Thoresen ◽

Maja Elstad

Keyword(s):

Stroke Volume ◽

Non Invasive ◽

Cardiac Stroke Volume

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In-vivo validation of a new non-invasive continuous ventricular stroke volume monitoring system in an animal model

Critical Care ◽

10.1186/cc10306 ◽

2011 ◽

Vol 15 (4) ◽

pp. R165 ◽

Cited By ~ 3

Author(s):

Maurits K Konings ◽

Paul F Grundeman ◽

Henk G Goovaerts ◽

Maarten R Roosendaal ◽

Imo E Hoefer ◽

...

Keyword(s):

Animal Model ◽

Stroke Volume ◽

Monitoring System ◽

Ventricular Stroke Volume ◽

Non Invasive ◽

In Vivo Validation

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The effect of progressive hypoxia on respiration in the dogfish (scyliorhinus canicula) at different seasonal temperatures

Journal of Experimental Biology ◽

10.1242/jeb.63.1.117 ◽

1975 ◽

Vol 63 (1) ◽

pp. 117-130 ◽

Cited By ~ 4

Author(s):

P. J. Butler ◽

E. W. Taylor

Keyword(s):

Heart Rate ◽

Cardiac Output ◽

Oxygen Uptake ◽

Stroke Volume ◽

Oxygen Tension ◽

Acclimation Temperature ◽

Critical Oxygen Tension ◽

Critical Oxygen ◽

Progressive Hypoxia ◽

Cardiac Stroke Volume

1. Dogfish were acclimated to 7, 12 or 17 degrees C and exposed to progressive hypoxia at the temperature to which they had been acclimated. During normoxia, the Q10 values for oxygen uptake, heart rate, cardiac output and respiratory frequency over the full 10 degrees C range were: 2.1, 2.1, 2.1 and 2.5 respectively. Increased acclimation temperature had no effect on cardiac stroke volume or systemic vascular resistance, although there was a decrease in branchial vascular resistance, pHa and pHv. 2. Progressive hypoxia had no effect on heart rate or oxygen uptake at 7 degrees C, whereas at 12 degrees C and 17 degrees C there was bradycardia, and a reduction in O2 uptake, with the critical oxygen tension for both variables being higher at the higher temperature. Cardiac stroke volume increased during hypoxia at each temperature, such that cardiac output did not change significantly at 12 and 17 degrees C. Neither pHa nor pHv changed significantly during hypoxia at any of the three temperatures. 3. The influence of acclimation temperatures on experimental results from poikilotherms is pointed out. Previously-published results show quantitative differences. 4. The significance of the present results with respect to the functioning and location of oxygen receptors is discussed. It is argued that as the metabolic demand and critical oxygen tension of the whole animal are increased at high acclimation temperatures the same must be the case with the oxygen receptor. This would raise the stimulation threshold and could account for the bradycardia seen during hypoxia becoming manifest at higher values of PI,O2, Pa,O2 and Pv,O2 as the acclimation temperature is raised.

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MECHANICAL PERFORMANCE OF AN IN SITU PERFUSED HEART FROM THE TURTLE CHRYSEMYS SCRIPTA DURING NORMOXIA AND ANOXIA AT 5 C AND 15 C

Journal of Experimental Biology ◽

10.1242/jeb.191.1.207 ◽

1994 ◽

Vol 191 (1) ◽

pp. 207-229 ◽

Cited By ~ 16

Author(s):

A Farrell ◽

C Franklin ◽

P Arthur ◽

H Thorarensen ◽

K Cousins

Keyword(s):

Heart Rate ◽

Cardiac Output ◽

Stroke Volume ◽

Power Output ◽

Mechanical Performance ◽

Perfused Heart ◽

Inotropic Effects ◽

Ventricular Mass

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.

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

Journal of Experimental Biology ◽

10.1242/jeb.199.3.663 ◽

1996 ◽

Vol 199 (3) ◽

pp. 663-672 ◽

Cited By ~ 23

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.

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