Atrioventricular Canal
Atrioventricular Canal - Related Videos
06:26
Capturing Flow-weighted Water and Suspended Particulates from Agricultural Canals During Drainage Events
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Cited by 2 •
2017
Nutrients present in particulate form can contribute significantly to the overall loads in agricultural drainage waters. This study describes a novel method to capture flow-weighted water and suspended particulates from farm canal drainage over the entire duration of the drainage event.
11:00
Biaxial Mechanical Characterizations of Atrioventricular Heart Valves
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Cited by 25 •
2019
This protocol involves characterizations of atrioventricular valve leaflets with force-controlled, displacement-controlled, and stress-relaxation biaxial mechanical testing procedures. Results acquired with this protocol can be used for constitutive model development to simulate the mechanical behavior of functioning valves under a finite element simulation framework.
08:38
Testing of all Six Semicircular Canals with Video Head Impulse Test Systems
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Cited by 26 •
2019
This protocol describes how to correctly perform the video head impulse test with two separate test systems commonly used worldwide. Both the 2D and 3D video head impulse test methods are described.
10:30
The C. elegans Excretory Canal as a Model for Intracellular Lumen Morphogenesis and In Vivo Polarized Membrane Biogenesis in a Single Cell: labeling by GFP-fusions, RNAi Interaction Screen and Imaging
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Cited by 6 •
2017
The C. elegans excretory canal is a unique single-cell model for the visual in vivo analysis of de novo polarized membrane biogenesis. This protocol describes a combination of standard genetic/RNAi and imaging approaches, adaptable for the identification and characterization of molecules directing unicellular tubulogenesis, and apical membrane and lumen biogenesis.
08:43
Isolation and Culture of Resident Cardiac Macrophages from the Murine Sinoatrial and Atrioventricular Node
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Cited by 4 •
2021
The protocol presented here provides a step-by-step approach for the isolation of cardiac resident macrophages from the sinoatrial node (SAN) and atrioventricular node (AVN) region of mouse hearts.
FAQs
During epithelial-to-mesenchymal transition, or EMT, endocardial cushion cells change from an epithelial arrangement into mesenchymal tissue. Together with cell proliferation, this supplies the cellular material needed for later remodeling of the common canal. The transition therefore links cellular behavior to formation of the structures that separate atrioventricular pathways.
Cell proliferation expands the cushion tissue, while remodeling organizes that tissue into functional cardiac structures. Neither process alone is sufficient: increased cell number must be followed by spatial reorganization that divides the common canal and contributes to valve and septal formation. Their coordination supports separate chambers and controlled blood movement.
Remodeling creates distinct right and left atrioventricular openings rather than leaving a single common passage. These openings align with the developing chambers and contribute to the mitral and tricuspid valves. As the chambers become separated, this structural arrangement helps establish one-way blood flow through the developing heart.
An atrioventricular septal defect can result when endocardial cushion formation or remodeling is incomplete. Because the cushions contribute to openings, valves, and septa, inadequate development can leave cardiac structures improperly separated. The resulting anatomical disruption provides a developmental explanation for abnormal atrioventricular organization and flow.
A useful sequence begins with endocardial cushion cell proliferation and epithelial-to-mesenchymal transition, then follows tissue formation, division of the common canal, and remodeling into separate openings. Researchers can next relate these changes to valve and septal contributions, chamber separation, and the establishment of one-way flow.
Analysis can show whether the common canal has been divided into right and left atrioventricular openings and whether cushion-derived tissue contributes appropriately to the mitral and tricuspid valves and septa. These outcomes connect microscopic developmental events with the larger cardiac architecture required for separated chambers and directed flow.
This developmental process provides a framework for linking cell behavior with congenital heart disease. Researchers can compare normal cushion formation and remodeling with incomplete development associated with atrioventricular septal defects. Such comparisons help clarify how structural abnormalities arise and support investigation of mechanisms and therapies for congenital cardiac disorders.