ABSTRACT
BACKGROUND/AIMS: Ligating the right lateral vitelline vein of chicken embryos (venous clip) results in cardiovascular malformations. These abnormalities are similar to malformations observed in knockout mice studies of components of the endothelin-1 (ET-1)/endothelin-converting enzyme-1/endothelin-A receptor pathway. In previous studies we demonstrated that cardiac ET-1 expression is decreased 3 h after clipping, and ventricular diastolic filling is disturbed after 2 days. Therefore, we hypothesise that ET-1-related processes are involved in the development of functional and morphological cardiovascular defects after venous clip. METHODS: In this study, ET-1 and endothelin receptor antagonists (BQ-123, BQ-788 and PD145065) were infused into the HH18 embryonic circulation. Immediate haemodynamic effects on the embryonic heart and extra-embryonic vitelline veins were examined by Doppler and micro-particle image velocimetry. Ventricular diastolic filling characteristics were studied at HH24, followed by cardiovascular morphologic investigation (HH35). RESULTS: ET-1 and its receptor antagonists induced haemodynamic effects at HH18. At HH24, a reduced diastolic ventricular passive filling component was demonstrated, which was compensated by an increased active filling component. Thinner ventricular myocardium was shown in 42% of experimental embryos. CONCLUSION: We conclude that cardiovascular malformations after venous clipping arise from a combination of haemodynamic changes and altered gene expression patterns and levels, including those of the endothelin pathway.
Subject(s)
Cardiovascular Abnormalities/metabolism , Endothelin-1/metabolism , Heart/physiopathology , Hemodynamics , Myocardium/metabolism , Receptors, Endothelin/metabolism , Signal Transduction , Yolk Sac/blood supply , Animals , Aspartic Acid Endopeptidases/genetics , Aspartic Acid Endopeptidases/metabolism , Blood Flow Velocity , Cardiac Output , Cardiovascular Abnormalities/genetics , Cardiovascular Abnormalities/pathology , Cardiovascular Abnormalities/physiopathology , Cells, Cultured , Chick Embryo , Echocardiography , Endothelin Receptor Antagonists , Endothelin-1/genetics , Endothelin-Converting Enzymes , Gene Expression Regulation, Developmental , Heart/embryology , Heart Rate , Hemodynamics/drug effects , Laser-Doppler Flowmetry , Ligation , Metalloendopeptidases/genetics , Metalloendopeptidases/metabolism , Myocardium/pathology , Oligopeptides/pharmacology , Peptides, Cyclic/pharmacology , Piperidines/pharmacology , RNA, Messenger/metabolism , Receptors, Endothelin/genetics , Signal Transduction/drug effects , Time Factors , Veins/physiopathology , Veins/surgery , Ventricular FunctionABSTRACT
We present the results of an experimental investigation into the nature and structure of turbulent pipe flow at moderate Reynolds numbers. A turbulence regeneration mechanism is identified which sustains a symmetric traveling wave within the flow. The periodicity of the mechanism allows comparison to the wavelength of numerically observed exact traveling wave solutions and close agreement is found. The advection speed of the upstream turbulence laminar interface in the experimental flow is observed to form a lower bound on the phase velocities of the exact traveling wave solutions. Overall our observations suggest that the dynamics of the turbulent flow at moderate Reynolds numbers are governed by unstable nonlinear traveling waves.
ABSTRACT
An in vitro model using a parallel-plate fluid flow chamber is supposed to simulate in vivo fluid shear stresses on various cell types exposed to dynamic fluid flow in their physiological environment. The metabolic response of cells in vitro is associated with the wall shear stress. However, parallel-plate flow chambers have not been characterized for dynamic fluid flow experiments. We use a dimensionless ratio h / lambda(v), in determining the exact magnitude of the dynamic wall shear stress, with its oscillating components scaled by a shear factor T. It is shown that, in order to expose cells to predictable levels of dynamic fluid shear stress, two conditions have to be met: (1) h / lambda(v) < 2, where h is the distance between the plates and lambda(v) is the viscous penetration depth; and (2) f(0) < f(c) / m, where the critical frequency f(c) is the upper threshold for this flow regime, m is the highest harmonic mode of the flow, and f(0) is the fundamental frequency of fluid flow.
Subject(s)
Body Fluids/physiology , Cell Physiological Phenomena , Models, Biological , Physiology/instrumentation , Animals , Computer Simulation , Differential Threshold , Equipment Design , Humans , Stress, Mechanical , ViscosityABSTRACT
Transition to turbulence in pipe flow is one of the most fundamental and longest-standing problems in fluid dynamics. Stability theory suggests that the flow remains laminar for all flow rates, but in practice pipe flow becomes turbulent even at moderate speeds. This transition drastically affects the transport efficiency of mass, momentum, and heat. On the basis of the recent discovery of unstable traveling waves in computational studies of the Navier-Stokes equations and ideas from dynamical systems theory, a model for the transition process has been suggested. We report experimental observation of these traveling waves in pipe flow, confirming the proposed transition scenario and suggesting that the dynamics associated with these unstable states may indeed capture the nature of fluid turbulence.
