title: The complex dielectric spectrum of heart tissue during ischemia.
abstract: BACKGROUND
  Because of the variety of tissue structures, the interpretation of the passive complex dielectric permittivity spectrum epsilon (omega) of the heart is still a problem. The aim of this work was to correlate epsilon (omega) of heart tissue with physical processes on cellular level.
  
  
  METHODS
  epsilon (omega) 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 epsilon (omega), we present two heart models which consider cell shape, electrical cell coupling, and dielectric polarisation of cell membranes and membranes of intracellular structures.
  
  
  RESULTS
  epsilon (omega) of heart tissue shows an alpha-, beta-, and gamma-dispersion. epsilon (omega) remains unchanged during cardioplegic perfusion with HTK, but if heptanol is added, there is an immediate decrease in the region of alpha-dispersion and an increase in the low frequency part of beta-dispersion. Similar changes are observed during ischemia following HTK perfusion without heptanol; additionally, the beta-dispersion shifts to higher frequencies. Using our models, we obtain analogue changes of epsilon (omega) by fitting model parameters which describe water content, water distribution, extra- and intracellular conductivity, and gap junction resistance.
  
  
  CONCLUSIONS
  Changes of these tissue properties as calculated by our models based on the measurement of epsilon (omega) 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.
authors.affiliation: Department of Experimental Surgery, University of Heidelberg, INF 365, D-69120 Heidelberg, Germany. michael.schaefer@exchi.uni-heidelberg.de
authors.forename: M
authors.initials: M
authors.lastname: Schaefer
authors.forename: W
authors.initials: W
authors.lastname: Gross
authors.forename: J
authors.initials: J
authors.lastname: Ackemann
authors.forename: M M
authors.initials: MM
authors.lastname: Gebhard
mesh_terms: D000818:Animals; D004285:Dogs; D017097:Electric Impedance; D017629:Gap Junctions / Q000473:pathology; D066298:In Vitro Techniques; D008929:Mitochondria, Heart / Q000502:physiology; D008933:Mitochondrial Swelling / Q000502:physiology; D008954:Models, Biological; D017202:Myocardial Ischemia / Q000473:pathology* / Q000503:physiopathology; D009206:Myocardium / Q000473:pathology*