Abstract
AimsWhile zebrafish embryos are amenable to in vivo imaging, allowing the study of morphogenetic processes during development, intravital imaging of adults is hampered by their small size and loss of transparency. The use of adult zebrafish as a vertebrate model of cardiac disease and regeneration is increasing at high speed. It is therefore of great importance to establish appropriate and robust methods to measure cardiac function parameters.Methods and ResultsHere we describe the use of 2D-echocardiography to study the fractional volume shortening and segmental wall motion of the ventricle. Our data show that 2D-echocardiography can be used to evaluate cardiac injury and also to study recovery of cardiac function. Interestingly, our results show that while global systolic function recovered following cardiac cryoinjury, ventricular wall motion was only partially restored.ConclusionCryoinjury leads to long-lasting impairment of cardiac contraction, partially mimicking the consequences of myocardial infarction in humans. Functional assessment of heart regeneration by echocardiography allows a deeper understanding of the mechanisms of cardiac regeneration and has the advantage of being easily transferable to other cardiovascular zebrafish disease models.
Highlights
Adult mammalian cardiomyocytes possess a limited capacity for self-renewal in homeostatic and pathologic situations [1, 2]
We have determined that the average fractional volume shortening (FVS) in adult zebrafish is 39¡5% in uninjured animals (n547, Fig. 1D, S1 Movie and S2 Movie)
We first sought to determine the variability in echocardiography measurements taken at different days, in order to establish basal physiological changes in cardiac function
Summary
Adult mammalian cardiomyocytes possess a limited capacity for self-renewal in homeostatic and pathologic situations [1, 2]. Myocardial infarction (MI), the most common cause of cardiac injury in humans, results in acute loss of large numbers of cardiomyocytes that are substituted by scar tissue [3]. This scar provides mechanical support to the infarcted heart, preventing wall rupture during the post-infarction period, scarring progressively leads to changes in ventricular geometry, referred to as ‘‘ventricular remodeling’’, which can lead to cardiac failure. Models of cardiac insult in the zebrafish include ventricular resection [5, 6] in addition to strategies that induce cell death rather than tissue removal, such as ventricular cryoinjury [7,8,9] or genetic ablation of cardiomyocytes [10]
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