Abstract
Aim of this study was to provide an echocardiographic protocol for the description of the normal murine venous reservoir (atrium, appendage and pulmonary veins) and to investigate the possibility to use this approach to discriminate changes on left atrium (LA) and left atrial appendage (LAA) in a stress-induced model such us myocardial infarction. Global left ventricular function and the venous reservoir were assessed by a Vevo2100 in 20 female C57BL/6N. LA and LAA were also studied in 10 CD-1 and 10 FVB mice, whereas modifications investigated in 15 C57BL/6N subjected to coronary artery ligation. Left ventricle function was evaluated as well as pulsed Doppler mitral valve, pulmonary vein, and LAA velocities. From 2D view monoplane LA volumes were obtained and LAA long axis measured. Macroscopic inspection with casts and immunohistochemistry were performed. Results show that compared to humans, in C57BL/6N mice left atrium was disproportionately smaller (5.2±1.4μL) than the left ventricle (53±8μL) and connected through a duct by a large LAA and posteriorly to three pulmonary veins. The LA volume increased 2-fold during reservoir with two distinct phases, early and late divided by a short pause. LAA long axis (4.1±0.5mm) was almost 2 times longer than the LA. LAA flow volume together with LA volume reservoir account for about 36% of stroke volume and the rest was provided by conduit flow. Linear regressions showed that stroke volume was strongly influenced by LAA flow, LA early filling volume and left ventricle base descent. Moreover, we also report the ability to assess LA and LAA in other mice strains and discriminate size increase following myocardial infarction. In conclusion, we performed a complete characterization of murine left venous reservoir establishing an optimized protocol that can be used in both investigative and pharmacological studies requiring rapid and serial determination of cardiac structure and function.
Highlights
Rodents are a powerful experimental model for a mechanistic understanding of normal cardiovascular function and to identify the molecular mechanisms underlying the pathological basis of cardiovascular diseases
The left atrium (LA) acts as a venous reservoir during left ventricle (LV) systole [3], enhances LV filling during early diastole, and contracts at end diastole to maximize LV end-diastolic volume and optimize stroke volume (SV)
Strong evidence suggest that the left atrial enlargement can be used as clinical indicator of significant risk of adverse cardiovascular outcomes for the patient, to investigate the possibility to use LA size as prognostic value, an understanding of the LA structure and function in animal models and its association with cardiovascular disease is required
Summary
Rodents are a powerful experimental model for a mechanistic understanding of normal cardiovascular function and to identify the molecular mechanisms underlying the pathological basis of cardiovascular diseases. Normal reference values have been established for murine left ventricle (LV) [1, 2] on the contrary, left atrium (LA) structure and function have never been evaluated. The LA acts as a venous reservoir during LV systole [3], enhances LV filling during early diastole, and contracts at end diastole to maximize LV end-diastolic volume and optimize stroke volume (SV). Recent advances in imaging technology provide improved spatial and temporal resolution to visualize rodent myocardium, allowing the investigation of its smallest structures. The overall goal of the present study was to provide an optimized acquisition and analysis protocol for the assessment of anatomy and function of the murine left venous reservoir. Functional and geometric changes were provided in a “stress-induced” model of myocardial infarction
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