Agnès Drochon

Interactions between red blood cells and a lethal, partly quaternized tertiary polyamine.

Partially quaternized poly[thio-1-(N,N-diethyl-aminomethyl) ethylene]s, Q-P(TDAE)(x) with x indicating the percentage of quaternized subunits, have been proposed as potential carriers for drugs insoluble in water. However these cationic polyelectrolytes form emboli upon intravenous administration. In order to study the mechanism, Q-P(TDAE)(11) was incubated in vitro with red blood cells (RBCs) suspended in various aqueous media such as autologous plasma, autologous serum, albumin dissolved in phosphate buffer, plasma-serum mixtures and Tris buffer. The deformability of the RBC membrane studied by viscometry was not affected by the polycation. Q-P(TDAE)(11)-induced hemagglutination was studied by optical microscopy. It depended on the polymer concentration and on the presence of plasma proteins. As ghosts were formed in some cases, hemolysis was investigated by measuring potassium and hemoglobin released from RBCs. Fibrinogen and serum proteins, except albumin, protected RBCs from hemolysis. Moreover the order of addition of the suspension components modulated dramatically the Q-P(TDAE)(11)-induced hemolysis. Addition of Q-P(TDAE)(11) to whole blood caused hemolysis whereas addition of the polymer to plasma prior to contact with RBCs did not affect the cell integrity. In contrast, addition of the polymer to RBCs suspended in albumin solution caused greater hemolysis than the addition to whole blood, and the contact between Q-P(TDAE)(11) and albumin prior to RBC addition still enhanced cell lysis. Two conclusions can be drawn from these observations: (i) Q-P(TDAE)(11) induces both hemagglutination, probably through electrostatic interaction, and hemolysis, because Q-P(TDAE)(11) disrupted the RBC lipid bilayer; (ii) proteins can decrease or increase the deleterious effects of Q-P(TDAE)(11) on RBCs.

Magnetohemodynamics effect on electrocardiograms

In presence of a high magnetic field, the blood flow in the aorta induces an electrical potential which is responsible for an increase of the T-wave in the electrocardiogram (ECG). This phenomenon may perturb ECG-gated imaging. The aim of this numerical study is to reproduce this experimental observation through computer simulations. The proposed model consists of three components: magnetohydrodynamics (MHD) in the aorta, bidomain equations in the heart and electrical diffusion in the rest of the body. These models are strongly coupled together and solved with finite elements. Some numerical results without and with a magnetic field are presented and discussed. When the magnetic field increases from B = 0T to B = 3T, it is observed numerically that the potential in the lead I of the ECG doubles during the T-wave, reaching the level of the QRS peak. All numerical computations were performed on a realistic averaged human model.

MAGNETOHYDRODYNAMIC FLOW OF BLOOD: INFLUENCE OF THE SIMPLIFYING ASSUMPTIONS IN CALCULATIONS

The movement of a conducting fluid, such as the blood, in an externally applied magnetic field, B0, is governed by the laws of magnetohydrodynamics. When the body is subjected to a magnetic field, as it is the case in magnetic resonance imaging (MRI), the charged particles of the blood flowing transversally to the field get deflected by the Lorentz force thus inducing electrical currents and voltages across the vessel walls and in the surrounding tissues, strong enough to be detected at the surface of the thorax in the electrocardiogram. Moreover, the interactions between these induced currents and the applied magnetic field can cause a reduction of flow rate and thus a reactive compensatory increase in blood pressure in order to retain a constant volume flow rate [Tenforde, 2005].

Stationary Flow of Blood in a Rigid Vessel in the Presence of an External Magnetic Field: Considerations about the Forces and Wall Shear Stresses

The magnetohydrodynamics laws govern the motion of a conducting fluid, such as blood, in an externally applied static magnetic field B0. When an artery is exposed to a magnetic field, the blood charged particles are deviated by the Lorentz force thus inducing electrical currents and voltages along the vessel walls and in the neighboring tissues. Such a situation may occur in several biomedical applications: magnetic resonance imaging (MRI), magnetic drug transport and targeting, tissue engineering… In this paper, we consider the steady unidirectional blood flow in a straight circular rigid vessel with non-conducting walls, in the presence of an exterior static magnetic field. The exact solution of Gold (1962) (with the induced fields not neglected) is revisited. It is shown that the integration over a cross section of the vessel of the longitudinal projection of the Lorentz force is zero, and that this result is related to the existence of current return paths, whose contributions compensate each other over the section. It is also demonstrated that the classical definition of the shear stresses cannot apply in this situation of magnetohydrodynamic flow, because, due to the existence of the Lorentz force, the axisymmetry is broken.