scholarly journals Can´t beat the heat? Importance of cardiac control and coronary perfusion for heat tolerance in rainbow trout

2019 ◽  
Vol 189 (6) ◽  
pp. 757-769 ◽  
Author(s):  
Andreas Ekström ◽  
Albin Gräns ◽  
Erik Sandblom
Keyword(s):  
Cardiac Output ◽  
Rainbow Trout ◽  
Heat Tolerance ◽  
Cardiac Failure ◽  
Cardiac Performance ◽  
Coronary Perfusion ◽  
Adrenergic Blockade ◽  
Adrenergic Stimulation ◽  
Autonomic Tone

Abstract Coronary perfusion and cardiac autonomic regulation may benefit myocardial oxygen delivery and thermal performance of the teleost heart, and thus influence whole animal heat tolerance. Yet, no study has examined how coronary perfusion affects cardiac output during warming in vivo. Moreover, while β-adrenergic stimulation could protect cardiac contractility, and cholinergic decrease in heart rate may enhance myocardial oxygen diffusion at critically high temperatures, previous studies in rainbow trout (Oncorhynchus mykiss) using pharmacological antagonists to block cholinergic and β-adrenergic regulation showed contradictory results with regard to cardiac performance and heat tolerance. This could reflect intra-specific differences in the extent to which altered coronary perfusion buffered potential negative effects of the pharmacological blockade. Here, we first tested how cardiac performance and the critical thermal maximum (CTmax) were affected following a coronary ligation. We then assessed how these performances were influenced by pharmacological cholinergic or β-adrenergic blockade, hypothesising that the effects of the pharmacological treatment would be more pronounced in coronary ligated trout compared to trout with intact coronaries. Coronary blockade reduced CTmax by 1.5 °C, constrained stroke volume and cardiac output across temperatures, led to earlier cardiac failure and was associated with reduced blood oxygen-carrying capacity. Nonetheless, CTmax and the temperatures for cardiac failure were not affected by autonomic blockade. Collectively, our data show that coronary perfusion improves heat tolerance and cardiac performance in trout, while evidence for beneficial effects of altered cardiac autonomic tone during warming remains inconclusive.

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.

Abstract 65: β-Adrenergic Signaling Promotes Survival and Proliferation of Mouse Cardiac Progenitor Cells Prior to Lineage Commitment

2012 ◽  
Vol 111 (suppl_1) ◽  
Author(s):  
Mohsin Khan ◽  
Sadia Mohsin ◽  
Daniele Avitabile ◽  
Jonathan Nguyen ◽  
Natalie Gude ◽  
...  
Keyword(s):  
Recovery Of Function ◽  
Cardiac Contractility ◽  
Stem Cell Marker ◽  
Adrenergic Blockade ◽  
Adrenergic Stimulation ◽  
Myocardial Repair ◽  
Akt Phosphorylation ◽  
Failing Heart

Rationale: Short term β-adrenergic stimulation promotes contractility in response to stress, but is ultimately detrimental in the failing heart due to accrual of cardiomyocyte death. Endogenous myocardial repair may partially offset cardiomyocyte losses, but consequences of long term β-adrenergic drive upon myocardial repair and regeneration are unknown. Objective: Modest recovery of cardiac contractility following long term β-adrenergic blockade in the clinical setting may depend, in part, upon restoration of endogenous repair therefore we sought to determine the relationship between β-adrenergic activity and regulation of cardiac progenitor cell (CPC) function and influence upon myocardial repair. Methods and results: Mouse and human CPCs express only β2 adrenergic receptor (β2-AR) in conjunction with stem cell marker c-kit. Activation of β2-AR signaling promotes proliferation associated with increased Akt phosphorylation, up-regulation of eNOS and cyclin D1, and decreased levels of GRK2. Conversely, silencing of β2-AR expression or treatment with β2-antagonist ICI 118, 551 impairs proliferation and survival. β1-AR expression in CPC is induced by differentiation stimuli, sensitizing CPC to isoproterenol-induced cell death that is abrogated by the β1-AR specific antagonist metoprolol. Efficacy of β1-AR blockade by metoprolol to increase CPC survival and proliferation was confirmed in vivo by adoptive transfer of CPC into failing mouse myocardium, concomitant with increased ejection fraction, fractional shortening and hemodynamic performance. Conclusions: β-adrenergic stimulation promotes expansion and survival of CPCs through β2-AR, but acquisition of β1-AR upon commitment to the myocyte lineage results in loss of early myocyte precursors and ineffective myocardial repair. Thus, β1-AR-specific blockade is likely to provide for enhanced CPC participation in recovery of function in the failing heart.

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 In vivo analysis of partitioning of cardiac output between systemic and central venous sinus circuits in rainbow trout: a new approach using chronic cannulation of the branchial vein

1988 ◽  
Vol 137 (1) ◽  
pp. 75-88 ◽  
Author(s):  
A. Ishimatsu ◽  
G. K. Iwama ◽  
N. Heisler
Keyword(s):  
Cardiac Output ◽  
Rainbow Trout ◽  
Venous Blood ◽  
Venous Sinus ◽  
Central Venous ◽  
Plasma Skimming ◽  
In Vivo Analysis ◽  
Chronic Cannulation

Freshwater-acclimated rainbow trout were chronically and non-occlusively cannulated in the dorsal aorta (DA), sinus venosus (SV) and branchial vein (BV), the latter returning the blood perfusing the central venous sinus (CVS) of the gill after being shunted away from the systemic circuit. After recovery, blood samples from these three sites were analysed for haematocrit (Hct) and [Hb]. Branchial venous blood was found to have considerably lower Hct and [Hb] (Hct = 3.5 +/− 3.1%; [Hb] = 1.04 +/− 0.75 g 100 ml-1) than systemic blood (DA: Hct = 24.3 +/− 8.9%, [Hb] = 6.54 +/− 2.90 g 100 ml-1; SV: Hct = 23.1 +/− 8.8%, [Hb] = 6.15 +/− 2.55 g 100 ml-1; means +/− S.D. N = 8), which strongly suggests that plasma skimming occurred at arteriovenous anastomoses and arterioles draining into the CVS. The partitioning of cardiac output, calculated on the basis of the [Hb] data, showed that the systemic flow accounted for 93 +/− 4.6% (N = 7) of the total cardiac output with only 7 +/− 4.7% of cardiac output being diverted into the CVS, thus bypassing the systemic vasculature. Previous results using in vitro experiments are compared with the present data in an evaluation of the usefulness of the isolated perfused gill and head preparations in the experimental analysis of circulatory physiology in fish gills.

Cardiovascular dynamics and adrenergic responses of the rainbow trout in vivo

1980 ◽  
Vol 87 (1) ◽  
pp. 247-270
Author(s):  
C. M. Wood ◽  
G. Shelton
Keyword(s):  
Cardiac Output ◽  
Pressor Response ◽  
Peripheral Resistance ◽  
Circulatory System ◽  
Receptor Activation ◽  
Cardiac Response ◽  
Positive Pressure ◽  
Adrenergic Blockade ◽  
Adrenergic Agents

Cardiac output and dorsal aorta, ventral aorta, caudal artery, caudal vein, and subintestinal vein pressures have been directly measured in intact unanaesthetized trout. Cardiac output (Q) averaged 36.7 ml/kg.min. The pressure drop across the systemic vascular resistance (Rs) was approximately twice that across the gill resistance (Rg), and a significant positive pressure persisted in the venous system. alpha-Adrenergic blockade revealed a considerable endogenous vasomotor tone resulting from latent adrenergic constriction of Rs. Intravenous adrenaline caused a pressor response throughout the circulatory system which has been analysed in detail with the aid of previous studies on isolated parts of the trout circulation. The complex and variable form of the pressor response reflected differential contributions from changes in Q, Rg, and Rs. Increases in Rs (alpha-receptor activation) were the principal cause of all pressor responses. Rg usually declined slightly due to passive dilation and/or beta-receptor stimulation, but occasionally increased due to alpha-receptor activation. The cardiac response reflected a varying balance between a direct beta-stimulatory effect of adrenaline on Q and an indirect passive inhibition of Q by the increase in peripheral resistance. Both effects were mediated through changes in stroke volume. Occasional tachycardia or more frequent reflex bradycardia were minor components of the cardiac response. The in vivo actions of other adrenergic agents have been similarly analysed.

Dynamic synchronization analysis of venous pressure-driven cardiac output in rainbow trout

2003 ◽  
Vol 285 (4) ◽  
pp. R889-R896 ◽  
Author(s):  
Adrienne Robyn Minerick ◽  
Hsueh-Chia Chang ◽  
Todd M. Hoagland ◽  
Kenneth R. Olson
Keyword(s):  
Cardiac Output ◽  
Rainbow Trout ◽  
Blood Volume ◽  
Hilbert Transform ◽  
Venous Pressure ◽  
Time Lag ◽  
Venous Compliance ◽  
Pressure Transducers ◽  
The Hilbert Transform

Measurement of venous function in vivo is inherently difficult. In this study, we used the Hilbert transform to examine the dynamic relationships between venous pressure and cardiac output (CO) in rainbow trout whose blood volume was continuously increased and decreased by ramp infusion and withdrawal (I/W). The dorsal aorta and ductus Cuvier were cannulated percutaneously and connected to pressure transducers; a flow probe was placed around the ventral aorta. Whole blood from a donor was then I/W via the dorsal aortic cannula at a rate of 10% of the estimated blood volume per minute, and the duration of I/W was varied from 40, 60, 80, 90, 120, 230, 240, 260, 300, and 340 s. Compliance [change in (Δ) blood vol/Δvenous pressure] was 2.8 ± 0.2 ml · mmHg-1 · g-1 ( N = 25 measurements; 6 fish with closed pericardium) and 2.8 ± 0.3 ml · mmHg-1 · kg-1 ( N = 19 measurements, 4 fish with open pericardium). Compliance was positively correlated with the duration of I/W, indicative of cardiovascular reflex responses at longer I/W durations. In trout with closed pericardium, CO followed venous pressure oscillations with an average time lag of 4.2 ± 1.0 s ( N = 9); heart rate (HR) was inversely correlated with CO. These studies show that CO is entrained by modulation of venous pressure, not by HR. Thus, although trout have a rigid pericardium, venous pressure (vis-a-tergo), not cardiac suction (vis-a-fronte), appears to be the primary determinant of CO. Estimation of venous compliance by ramp-modulation of venous pressure is faster and less traumatic than classical capacitance measurements and appears applicable to a variety of vertebrate species, as does the Hilbert transform, which permits analysis of signals with disparate frequencies.

scholarly journals Cardiac disease in mucopolysaccharidosis type I attributed to catecholaminergic and hemodynamic deficiencies

2011 ◽  
Vol 300 (1) ◽  
pp. H356-H365 ◽  
Author(s):  
Nathan J. Palpant ◽  
Fikru B. Bedada ◽  
Brandon Peacock ◽  
Bruce R. Blazar ◽  
Joseph M. Metzger ◽  
...  
Keyword(s):  
Cardiac Output ◽  
Heart Function ◽  
Linear Regression Analysis ◽  
Type I ◽  
Mucopolysaccharidosis Type ◽  
Mucopolysaccharidosis Type I ◽  
Autonomic Tone ◽  
Cardiac Reserve ◽  
Mps I

Cardiac dysfunction is a common cause of death among pediatric patients with mutations in the lysosomal hydrolase α-l-iduronidase ( IDUA) gene, which causes mucopolysaccharidosis type I (MPS-I). The purpose of this study was to analyze adrenergic regulation of cardiac hemodynamic function in MPS-I. An analysis of murine heart function was performed using conductance micromanometry to assess in vivo cardiac hemodynamics. Although MPS-I ( IDUA −/−) mice were able to maintain normal cardiac output and ejection fraction at baseline, this cohort had significantly compromised systolic and diastolic function compared with IDUA +/− control mice. During dobutamine infusion MPS-I mice did not significantly increase cardiac output from baseline, indicative of blunted cardiac reserve. Autonomic tone, measured functionally by β-blockade, indicated that MPS-I mice required catecholaminergic stimulation to maintain baseline hemodynamics. Survival analysis showed mortality only among MPS-I mice. Linear regression analysis revealed that heightened end-systolic volume in the resting heart is significantly correlated with susceptibility to mortality in MPS-I hearts. This study reveals that cardiac remodeling in the pathology of MPS-I involves heightened adrenergic tone at the expense of cardiac reserve with cardiac decompensation predicted on the basis of increased baseline systolic volumes.

scholarly journals Influence of the coronary circulation on thermal tolerance and cardiac performance during warming in rainbow trout

2017 ◽  
Vol 312 (4) ◽  
pp. R549-R558 ◽  
Author(s):  
Andreas Ekström ◽  
Michael Axelsson ◽  
Albin Gräns ◽  
Jeroen Brijs ◽  
Erik Sandblom
Keyword(s):  
Heart Rate ◽  
Blood Flow ◽  
Rainbow Trout ◽  
Cardiac Function ◽  
Thermal Tolerance ◽  
Coronary Flow ◽  
Coronary Circulation ◽  
Cardiac Performance ◽  
Juvenile Trout

Thermal tolerance in fish may be related to an oxygen limitation of cardiac function. While the hearts of some fish species receive oxygenated blood via a coronary circulation, the influence of this oxygen supply on thermal tolerance and cardiac performance during warming remain unexplored. Here, we analyzed the effect in vivo of acute warming on coronary blood flow in adult sexually mature rainbow trout ( Onchorhynchus mykiss) and the consequences of chronic coronary ligation on cardiac function and thermal tolerance in juvenile trout. Coronary blood flow at 10°C was higher in females than males (0.56 ± 0.08 vs. 0.30 ± 0.08 ml·min−1·g ventricle−1), and averaged 0.47 ± 0.07 ml·min−1·g ventricle−1 across sexes. Warming increased coronary flow in both sexes until 14°C, at which it peaked and plateaued at 0.78 ± 0.1 and 0.61 ± 0.1 ml·min−1·g ventricle−1 in females and males, respectively. Thus, the scope for increasing coronary flow was 101% in males, but only 39% in females. Coronary-ligated juvenile trout exhibited elevated heart rate across temperatures, reduced Arrhenius breakpoint temperature for heart rate (23.0 vs. 24.6°C), and reduced upper critical thermal maximum (25.3 vs. 26.3°C). To further analyze the effects of coronary flow restriction on cardiac rhythmicity, electrocardiogram characteristics were determined before and after coronary occlusion in anesthetized trout. Occlusion resulted in reduced R-wave amplitude and an elevated S-T segment, indicating myocardial ischemia, while heart rate was unaffected. This suggests that the tachycardia in ligated trout across temperatures in vivo was mainly to compensate for reduced cardiac contractility to maintain cardiac output. Moreover, our findings show that coronary flow increases with warming in a sex-specific manner. This may improve whole animal thermal tolerance, presumably by sustaining cardiac oxygenation and contractility at high temperatures.

scholarly journals Adrenergic tone benefits cardiac performance and warming tolerance in two teleost fishes that lack a coronary circulation

2021 ◽  
Author(s):  
Andreas Ekström ◽  
Erika Sundell ◽  
Daniel Morgenroth ◽  
Erik Sandblom
Keyword(s):  
Heart Rate ◽  
Cardiac Function ◽  
High Temperatures ◽  
Oxygen Delivery ◽  
Thermal Tolerance ◽  
Heart Function ◽  
Perca Fluviatilis ◽  
Cardiac Performance ◽  
Adrenergic Stimulation

AbstractTolerance to acute environmental warming in fish is partly governed by the functional capacity of the heart to increase systemic oxygen delivery at high temperatures. However, cardiac function typically deteriorates at high temperatures, due to declining heart rate and an impaired capacity to maintain or increase cardiac stroke volume, which in turn has been attributed to a deterioration of the electrical conductivity of cardiac tissues and/or an impaired cardiac oxygen supply. While autonomic regulation of the heart may benefit cardiac function during warming by improving myocardial oxygenation, contractility and conductivity, the role of these processes for determining whole animal thermal tolerance is not clear. This is in part because interpretations of previous pharmacological in vivo experiments in salmonids are ambiguous and were confounded by potential compensatory increases in coronary oxygen delivery to the myocardium. Here, we tested the previously advanced hypothesis that cardiac autonomic control benefits heart function and acute warming tolerance in perch (Perca fluviatilis) and roach (Rutilus rutilus); two species that lack coronary arteries and rely entirely on luminal venous oxygen supplies for cardiac oxygenation. Pharmacological blockade of β-adrenergic tone lowered the upper temperature where heart rate started to decline in both species, marking the onset of cardiac failure, and reduced the critical thermal maximum (CTmax) in perch. Cholinergic (muscarinic) blockade had no effect on these thermal tolerance indices. Our findings are consistent with the hypothesis that adrenergic stimulation improves cardiac performance during acute warming, which, at least in perch, increases acute thermal tolerance.

EFFECT OF CORONARY ABLATION AND ADRENERGIC STIMULATION ON IN VIVO CARDIAC PERFORMANCE IN TROUT (ONCORHYNCHUS MYKISS)

1994 ◽  
Vol 186 (1) ◽  
pp. 127-143 ◽  
Author(s):  
A. Gamperl ◽  
A. Pinder ◽  
R. Boutilier
Keyword(s):  
Coronary Artery ◽  
Strong Relationship ◽  
Peripheral Circulation ◽  
Cardiac Performance ◽  
Post Injection ◽  
Adrenergic Stimulation ◽  
Post Surgery

In fish, catecholamine-induced changes in cardiac performance in vivo are the result of complex interactions between the direct adrenergic effects on the heart and peripheral circulation and the reflex responses to increased blood pressure. In addition, coronary artery transport of catecholamines and oxygen to the compact myocardium may be essential for maximal in vivo cardiac performance during adrenergic stimulation. Cardiac output (Q(dot)), heart rate (fh), stroke volume (Vs) and dorsal aortic pressure (Pda) were measured in trout with intact or ablated coronary arteries at rest and following intra-arterial administration of 0.2, 0.5, 1.0 and 2.0 µg kg-1 adrenaline. Resting Q(dot), fh, Vs and Pda were the same in fish with intact and ablated coronaries at 48 h post-surgery, averaging approximately 18 ml min-1 kg-1, 42 beats min-1, 0.42 ml kg-1 and 2.2 kPa, respectively. All cardiovascular variables showed a strong relationship between response magnitude and adrenaline dose. However, our results indicate that adrenaline doses above 0.5 µg kg-1 may have a limited ability to increase Q(dot) (ED50 0.22 µg kg-1). Coronary artery ablation had little effect on post-injection Q(dot), Vs, Pda or fh at any dose of adrenaline. In both intact and ablated groups, two types of responses in Q(dot) were observed following adrenaline injection. In the ‘type 1′ response, Q(dot) increased shortly (15–30 s) after adrenaline administration, as increases in Vs more than compensated for a pressor-stimulated reflex bradycardia. In the ‘type 2′ response, alterations in Q(dot) were biphasic. In the initial minutes post-injection, Q(dot) fell and reached a minimum level at 1–2 min, the result of an immediate drop in fh and a delayed post-injection increase in Vs. Thereafter, Q(dot) gradually increased as a result of concordant increases in fh and Vs. Although time to maximum Q(dot) was 5–6 min longer for fish exhibiting type 2 responses, there was no difference in maximum Q(dot) increase or in the time courses for changes in fh and Pda between response types. Our results suggest (1) that during normoxic conditions, cardiac performance does not depend highly on coronary blood flow; (2) that the capacity of adrenaline to increase Q(dot) may be limited by elevations in output pressure and/or by the low dose (concentration) of adrenaline required to achieve near maximal adrenergic stimulation of the heart; and (3) that fish exhibiting type 2 responses have an increased barostatic gain (%delta fh per unit Pda) compared with those with type 1 responses.

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