Introduction

Many of the immediate clinical signs of electrical injury relate to neuromuscular damage. Intense muscular spasm and rigour are often described by witnesses and are frequently observed on admission to the hospital. These observations in addition to the release of myoglobin into the circulation suggest that muscle cell membranes are often ruptured by electrical trauma.

Bilayer–lipid membranes comprise 60% of cell membranes. When bilayer–lipid membranes are exposed to electric fields, their electrical conductivity and diffusive permeability increase. This process has been termed electroporation. The theory of electroporation assumes that thermally driven molecular defects or pores transiently form in bilayer–lipid membranes. These pores explain the ability of large molecules like glucose to permeate. When strong enough electric fields are imposed in the bilayer, the pores enlarge. If the pores become large enough, then the membrane ruptures.

Depending on the make-up of the membrane, the threshold transmembrane potential required to cause membrane rupture by electroporation ranges in amplitude from 300 mV to 500 mV and is 100 μs or more in duration. The resultant increase in transport allows substances which cannot normally permeate the membrane (e.g. DNA), to cross. Even localized rupture may spontaneously reseal. Electroporation can, therefore, be used for sequestering proteins, DNA, and various drugs into cells. During application of the voltage pulses, if the membranes of neighbouring cells are close enough, they may fuse to form a hybrid cell.

Because the membrane defects fill with water, determining the defect size is important in modelling the electrical properties of the membrane.