Release and uptake of haemoglobin and ions in red blood cells induced by dielectric breakdown

Abstract

External electric field strengths of the order of 10-3 minus10-4 v-cm-minus1 induce potassium release and concomitant sodium uptake in human and bovine red blood cells, as demonstrated in an electrolytic discharge chamber. The reversible increase of the membrane permeability once the critical membrane potential is reached is caused by dielectric breakdown of the membrane. The values of the critical membrane potential differences calculated from the potassium release and sodium uptake curves are close to those which were calculated from dielectric breakdown measurements in a hydrodynamic focussing Coulter Counter using the Laplace equation. With bovine red blood cells, the potassium release and the concomitant sodium uptake is coupled with haemoglobin release from the cells, while with human red blood cells much higher external electric field strengths are required for haemoglobin release. The external electric field strength required for solute release and uptake in bovine and human red blood cells depends on the pulse length, particularly below a value of about 10 mus, when a strong increase in the field strength occurs with decreasing pulse lengths. At 50-100 mus pulse lengths an asymptotic value of the critical electrical field strength of 2.6 kV-cm-minus1 for the modal volume of human red blood cells and 2.8 kV-cm-minus1 for the modal volume of bovine red blood cells is reached, corresponding to a critical membrane potential difference of about 1.1 V for both species. This value is close to that measured directly for dielectric breakdown of the membranes of Valonia utricularis (0.85 V, 20 degrees C). The increase in electric field strength with decreasing pulse length can be explained by the capacitance of the membrane, which becomes the rate limiting step for the temporal build-up of the electric potential across the membrane. The time constant of this process was determined to be approx. 10 mus. The critical membrane potential difference for breakdown is therefore pulse-length independent. The breakdown of the membrane can be interpreted by an electromechanical collapse of the membrane material. Numerical considerations of the dynamics of this membrane collapse predict that the breakdown time is a very rapid process.