Abstract

Introduction: Because of the variety of tissue structures, the interpretation of the passive complex dielectric permittivity spectrum ε( ω) of the heart is still a problem. The aim of this work was to correlate ε( ω) of heart tissue with physical processes on cellular level. Methods: ε( ω) of canine hearts was continuously measured in the range from 10 Hz to 400 MHz during cardioplegic perfusion and during following ischemia. Cardioplegic perfusion was performed with HTK (Custodiol®) without or with heptanol, in order to produce electrical cell uncoupling via the closure of gap junctions. To analyse ε( ω), we present two heart models which consider cell shape, electrical cell coupling, and dielectric polarisation of cell membranes and membranes of intracellular structures. Results: ε( ω) of heart tissue shows an α-, β-, and γ-dispersion. ε( ω) remains unchanged during cardioplegic perfusion with HTK, but if heptanol is added, there is an immediate decrease in the region of α-dispersion and an increase in the low frequency part of β-dispersion. Similar changes are observed during ischemia following HTK perfusion without heptanol; additionally, the β-dispersion shifts to higher frequencies. Using our models, we obtain analogue changes of ε( ω) by fitting model parameters which describe water content, water distribution, extra- and intracellular conductivity, and gap junction resistance. Discussion: Changes of these tissue properties as calculated by our models based on the measurement of ε( ω) are consistent with intraischemic changes of heart tissue known from immunohistochemical, biochemical, and histological investigations. The next step will be to use our models for the prognosis of irreversible tissue damage.

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