scholarly journals Cardioluminescence in Transgenic Zebrafish Larvae: A Calcium Imaging Tool to Study Drug Effects and Pathological Modeling

Biomedicines ◽  
2021 ◽  
Vol 9 (10) ◽  
pp. 1294
Author(s):  
Manuel Vicente ◽  
Jussep Salgado-Almario ◽  
Michelle M. Collins ◽  
Antonio Martínez-Sielva ◽  
Masafumi Minoshima ◽  
...  
Keyword(s):  
Heart Failure ◽  
Cardiac Output ◽  
Transgenic Line ◽  
Light Output ◽  
Study Drug ◽  
Calcium Oscillations ◽  
Transgenic Zebrafish ◽  
Calcium Dynamics ◽  
Cardiovascular Research ◽  
Zebrafish Larvae

Zebrafish embryos and larvae have emerged as an excellent model in cardiovascular research and are amenable to live imaging with genetically encoded biosensors to study cardiac cell behaviours, including calcium dynamics. To monitor calcium ion levels in three to five days post-fertilization larvae, we have used bioluminescence. We generated a transgenic line expressing GFP-aequorin in the heart, Tg(myl7:GA), and optimized a reconstitution protocol to boost aequorin luminescence. The analogue diacetyl h-coelenterazine enhanced light output and signal-to-noise ratio. With this cardioluminescence model, we imaged the time-averaged calcium levels and beat-to-beat calcium oscillations continuously for hours. As a proof-of-concept of the transgenic line, changes in ventricular calcium levels were observed by Bay K8644, an L-type calcium channel activator and with the blocker nifedipine. The β-adrenergic blocker propranolol decreased calcium levels, heart rate, stroke volume, and cardiac output, suggesting that larvae have a basal adrenergic tone. Zebrafish larvae treated with terfenadine for 24 h have been proposed as a model of heart failure. Tg(myl7:GA) larvae treated with terfenadine showed bradycardia, 2:1 atrioventricular block, decreased time-averaged ventricular calcium levels but increased calcium transient amplitude, and reduced cardiac output. As alterations of calcium signalling are involved in the pathogenesis of heart failure and arrhythmia, the GFP-aequorin transgenic line provides a powerful platform for understanding calcium dynamics.

scholarly journals Cardioluminescence in transgenic zebrafish embryos: a calcium imaging tool to study drug effects and pathological modeling

2021 ◽  
Author(s):  
Manuel Vicente ◽  
Jussep Salgado-Almario ◽  
Michelle M. Collins ◽  
Antonio Martinez-Sielva ◽  
Masafumi Minoshima ◽  
...  
Keyword(s):  
Signal To Noise Ratio ◽  
Light Output ◽  
Drug Effects ◽  
Study Drug ◽  
Transgenic Zebrafish ◽  
Zebrafish Embryos ◽  
Cardiovascular Research ◽  
Imaging Tool ◽  
Adrenergic Blocker

The zebrafish embryo has emerged as an excellent model in cardiovascular research. The existing techniques to monitor Ca2+ in the heart based on fluorescent Ca2+ biosensors are limited due to phototoxicity and photobleaching. To overcome these issues, we have used bioluminescence. We generated a transgenic line expressing GFP-Aequorin in the heart, Tg(cmlc2:GA), and optimized an in vivo aequorin reconstitution protocol to improve the luminescence capacity. This allowed imaging Ca2+ in long duration recordings in embryos of 3 to 5 days post-fertilization. The analogs diacetyl h-coelenterazine and f-coelenterazine enhanced the light output and signal-to-noise ratio from the embryos. With this cardioluminescence model, we monitored the time-averaged Ca2+ levels and beat-to-beat Ca2+ oscillations. Changes in Ca2+ levels were observed by incubation with BayK8644, an L-type Ca2+ channel agonist, the channel blocker nifedipine, and β-adrenergic blocker propranolol. Treatment of zebrafish embryos with terfenadine for 24 hours has been proposed as a model of heart failure. Tg(cmlc2:GA) embryos treated with terfenadine showed a 2:1 atrioventricular block and a decrease in the ventricular Ca2+ levels.

1406Inhaled iloprost, exercise hemodynamics, and ventricular performance in heart failure with preserved ejection fraction

2019 ◽  
Vol 40 (Supplement_1) ◽  
Author(s):  
J.-F Cheng ◽  
C.-K Wu ◽  
C.-Y Huang ◽  
Z.-W Chen ◽  
S.-Y Chen ◽  
...  
Keyword(s):  
Heart Failure ◽  
Cardiac Output ◽  
Ejection Fraction ◽  
Study Drug ◽  
Left Ventricular ◽  
Stroke Work ◽  
Preserved Ejection Fraction ◽  
Ventricular Performance ◽  
Inhaled Iloprost ◽  
Exercise Hemodynamics

Abstract Background A dramatic increase in pulmonary capillary wedge pressure (PCWP) during exercise is observed in patients with heart failure with preserved ejection fraction (HFpEF). The prostacyclin pathway is involved in pulmonary hypertension and iloprost is a prostacyclin analogue. The acute onset vasodilator effect of inhaled iloprost makes it a good candidate to decrease exercise-induced PCWP. This study determined whether iloprost inhalation could improve exercise hemodynamics and cardiac reserve in HFpEF. Methods Thirty-four HFpEF subjects were enrolled in this double-blind, randomized, placebo-controlled, parallel-group trial. Subjects received invasive cardiac catheterization and underwent expired gas analysis at rest and during exercise, before and 15 minutes after treatment with either inhaled iloprost or placebo. Results At baseline, enrolled subjects showed an increase in PCWP during exercise (PCWP = 16 (14–23) mmHg to 27 (21–36) mmHg; p<0.0001). After drug inhalation treatment, the primary endpoint was achieved whereby exercise PCWP was significantly reduced by iloprost compared to placebo (adjusted mean: 20 (16–29) mmHg vs. 23 (17–32) mmHg; p=0.002). Iloprost showed a trend for better cardiac output reserve with exercise (0.2 (−1.3 to 1.2) L/min vs. −0.7 (−1.9 to 0.1) L/min; p=0.099) and normalized the increase in cardiac output relative to oxygen consumption. Iloprost improved the pulmonary artery pressure flow relationships in HFpEF and showed a trend for increased left ventricular stroke work with exercise compared to placebo, indicating an improvement in ventricular performance with stress. Table shows exercise baseline-corrected values (exercise values after receiving study drug minus exercise values prior to study drug) Placebo (n=17) Iloprost (n=17) p Value PA systolic, mmHg 0 (−4 to 6) −11 (−23 to −5) <0.0001 PCWP, mmHg −2 (−3 to 2) −7 (−12 to −5) <0.0001 PVR, mmHg/l/min 0 (−0.5 to 0.3) −0.1 (−0.5 to 0.4) 0.9 SVR, DSC 102 (16 to 188) 5 (−162 to 108) 0.057 LVSW, g/beat −3 (−30 to 6) 7 (−13 to 20) 0.079 CO, l/min −0.7 (−1.9 to 0.1) 0.2 (−1.3 to 1.2) 0.099 Stroke volume, ml −8 (−24 to 1) 0 (−19 to 10) 0.3 Values are median (interquartile range). Conclusions Iloprost inhalation improved hemodynamic deficit during exercise in patients with HFpEF. Prospective trials testing long-term iloprost therapy in this population are warranted.

Heart Failure due to Tension Hydrothorax after Left Pneumonectomy

2013 ◽  
Vol 16 (6) ◽  
pp. 319 ◽  
Author(s):  
Kim Maguire ◽  
Calvin Leung ◽  
Visali Kodali ◽  
Brice Taylor ◽  
Jacques-Pierre Fontaine ◽  
...  
Keyword(s):  
Heart Failure ◽  
Cardiac Output ◽  
Rare Complication ◽  
Right Heart Failure ◽  
Symptomatic Improvement ◽  
Extrapleural Pneumonectomy ◽  
Pleural Mesothelioma ◽  
Low Cardiac Output ◽  
Mediastinal Shift ◽  
Left Pleural Effusion

Tension hydrothorax is a rare complication of pneumonectomy for pleural mesothelioma and an exceptionally rare cause of heart failure. We describe a patient who had undergone extrapleural pneumonectomy, chemotherapy, and radiation for pleural mesothelioma and who developed heart failure symptoms within months of the completion of treatment. Investigation showed a massive left pleural effusion resulting in tension hydrothorax, mediastinal shift, and evidence of right heart failure with constrictive physiology and low cardiac output. Therapeutic thoracentesis resulted in increase in cardiac output and symptomatic improvement.

scholarly journals Patterns of Comorbidity in Older Adults with Heart Failure: The Cardiovascular Research Network PRESERVE Study

2013 ◽  
Vol 61 (1) ◽  
pp. 26-33 ◽  
Author(s):  
Jane S. Saczynski ◽  
Alan S. Go ◽  
David J. Magid ◽  
David H. Smith ◽  
David D. McManus ◽  
...  
Keyword(s):  
Heart Failure ◽  
Older Adults ◽  
Research Network ◽  
Cardiovascular Research

Characterization of baroreflex impairment in conscious dogs with pacing-induced heart failure

1993 ◽  
Vol 265 (5) ◽  
pp. R1132-R1140 ◽  
Author(s):  
N. B. Olivier ◽  
R. B. Stephenson
Keyword(s):  
Heart Failure ◽  
Blood Pressure ◽  
Heart Rate ◽  
Cardiac Output ◽  
Peripheral Resistance ◽  
Open Loop ◽  
Ventricular Pacing ◽  
Baroreflex Control ◽  
Rapid Ventricular Pacing ◽  
Reflex Control

Open-loop baroreflex responses were evaluated in eight conscious dogs before and during congestive heart failure to determine the effects of failure on baroreflex control of blood pressure, heart rate, cardiac output, and total peripheral resistance. Heart failure was induced by rapid ventricular pacing. Baroreflex function was determined by calculation of the range and gain of the open-loop stimulus-response relationships for the effect of carotid sinus pressure on blood pressure, heart rate, cardiac output, and total peripheral resistance. The range and gain of blood pressure responses were substantially reduced as early as 3 days after induction of heart failure (161 +/- 6 to 99 +/- 8 mmHg and -2.7 +/- 0.3 to -1.5 +/- 0.1, respectively) and remained depressed for the 21 days of heart failure. This depression in baroreflex control of blood pressure was associated with similar depressions in reflex range and gain for heart rate (125 +/- 9 to 78 +/- 11 beats/min and -2.05 +/- 0.2 to -1.16 +/- 0.2 beats/min, respectively) and cardiac output (1.74 +/- 0.2 to 0.46 +/- 0.2 l/min and -0.81 +/- 0.02 to -0.027 +/- 0.008 l/min, respectively). The group-averaged range and gain for reflex control of vascular resistance were not altered by heart failure. In three dogs, discontinuation of rapid ventricular pacing led to resolution of heart failure within 7 days and partial restoration of the range and gain of reflex control of blood pressure. We conclude that heart failure reversibly depresses baroreflex control of blood pressure principally through a concurrent reduction in reflex control of cardiac output, whereas reflex control of vascular resistance is not consistently affected.

Redistribution of cardiac output during exercise by functional mitral regurgitation in heart failure: compensatory O2 peripheral uptake to delivery failure

2020 ◽  
Vol 319 (1) ◽  
pp. H100-H108
Author(s):  
Marco Guazzi ◽  
Greta Generati ◽  
Barry Borlaug ◽  
Eleonora Alfonzetti ◽  
Tadafumi Sugimoto ◽  
...  
Keyword(s):  
Heart Failure ◽  
Cardiac Output ◽  
Gas Exchange ◽  
Mitral Regurgitation ◽  
Functional Mitral Regurgitation ◽  
Functional Evaluation ◽  
Severe Mitral Regurgitation ◽  
Reduced Ejection Fraction ◽  
Heart Failure Patients ◽  
Fraction Versus

This is an analysis involving 134 heart failure patients with reduced ejection fraction versus 80 controls investigated during functional evaluation with gas exchange and hemodynamic, addressing the severe mitral regurgitation phenotype and testing the hypothesis that the backward cardiac output redistribution to the lung during exercise impairs delivery and overexpresses peripheral extraction. This information is new and has important implications in the management of heart failure.

scholarly journals Bioimpedance Vector Analysis for Heart Failure: Should We Put It on the Agenda?

2021 ◽  
Vol 8 ◽  
Author(s):  
Bo Liang ◽  
Rui Li ◽  
Jia-Yue Bai ◽  
Ning Gu
Keyword(s):  
Heart Failure ◽  
Cardiac Output ◽  
Clinical Diagnosis ◽  
Acute Decompensated Heart Failure ◽  
Decompensated Heart Failure ◽  
Clinical Syndrome ◽  
Vector Analysis ◽  
Diagnosis And Management ◽  
Volume Assessment ◽  
Intracardiac Pressure

Heart failure is a clinical syndrome, resulting in increased intracardiac pressure and/or decreased cardiac output under rest or stress. In acute decompensated heart failure, volume assessment is essential for clinical diagnosis and management. More and more evidence shows the advantages of bioimpedance vector analysis in this issue. Here, we critically present a brief review of bioimpedance vector analysis in the prediction and management of heart failure to give a reference to clinical physicians and guideline makers.

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