J Korean Med Sci.  2010 Apr;25(4):577-582. 10.3346/jkms.2010.25.4.577.

Bioelectrical Impedance May Predict Cell Viability During Ischemia and Reperfusion in Rat Liver

  • 1Research Institute of Biomedical Engineering, College of Medicine, Yeungnam University, Daegu, Korea.
  • 2Department of Physiology, College of Medicine, Yeungnam University, Daegu, Korea.
  • 3Department of Surgery, College of Medicine, Yeungnam University, Daegu, Korea.


Ischemia and reperfusion (I/R) injury is a major cause of hepatic failure after liver surgery, but no method could monitor or predict it real-time during surgery. We measured bioelectrical impedance (BEI) and cell viability to assess the usefulness of BEI during I/R in rat liver. A 70% partial liver ischemia model was used. BEI was measured at various frequencies. Adenosine triphosphate (ATP) content, and palmitic acid oxidation rate were measured, and histological changes were observed in order to quantify liver cell viability. BEI changed significantly during ischemia at low frequency. In the ischemia group, BEI increased gradually during 60 min of ischemia and had a tendency to plateau thereafter. The ATP content decreased below 20% of the baseline level. In the I/R group, BEI recovered to near baseline level. After 24 hr of reperfusion, the ATP contents decreased to below 50% in 30, 60 and 120 min of ischemia and the palmitic acid metabolic rates decreased to 91%, 78%, and 74%, respectively, compared with normal liver. BEI may be a good tool for monitoring I/R during liver surgery. The liver is relatively tolerant to ischemia, however after reperfusion, liver cells may be damaged depending upon the duration of ischemia.


Bioelectrical Impedance; Cell Survival; Ischemia; Reperfusion; ATP

MeSH Terms

Adenosine Triphosphate/metabolism
*Cell Survival
Electric Impedance
Energy Metabolism
Rats, Sprague-Dawley
Reperfusion Injury/metabolism/pathology
Adenosine Triphosphate


  • Fig. 1 Schematic diagram showing how bioelectrical impedance and temperature were measured in rat liver. We applied 70% ischemia model proposed by Camargo et al. (6).

  • Fig. 2 Bioelectrical impedance changes in the liver during 120 min of ischemia. *P<0.05 vs. 0 min (non-ischemia).

  • Fig. 3 ATP content of the liver during 120 min of ischemia. *P<0.05 vs. 0 min (non-ischemia); †P<0.05 vs. 30 min of ischemia.

  • Fig. 4 Palmitic acid oxidation rate of the liver during 120 min of ischemia.

  • Fig. 5 Histological findings in the liver during 120 min of ischemia. (A-D): H&E stain, ×40; (A1-D1): TUNEL stain, ×40; (A, A1): control; (B, B1): 30 min of ischemia; (C, C1): 60 min of ischemia; (D, D1): 120 min of ischemia.

  • Fig. 6 Bioelectrical impedance (0.12 KHz) changes in the liver during ischemia and reperfusion. Liver ischemia was maintained for 30, 60, and 120 min, respectively, and then reperfused for 60 min. *P<0.05 vs. 0 min (non-ischemia).

  • Fig. 7 ATP content of the liver after 24 hr of reperfusion, following 30, 60, and 120 min of ischemia. *P<0.05 vs. 0 min (non-ischemia); †P<0.05 vs. 30 min of ischemia.

  • Fig. 8 Palmitic acid oxidation rate of the liver after 24 hr of reperfusion following 30, 60, and 120 min of ischemia. *P<0.05 vs. 0 min (non-ischemia); †P<0.05 vs. 30 min of ischemia.

  • Fig. 9 Histological findings in the liver after 24 hr of reperfusion following 30, 60, and 120 min of ischemia. (A-C1): H&E stain, ×40; (A-C1): TUNEL stain, ×40; (A, A1): 30 min of ischemia and 24 hr of reperfusion; (B, B1): 60 min of ischemia and 24 hr of reperfusion; (C, C1): 120 min of ischemia and 24 hr of reperfusion.

Cited by  1 articles

Significance of Bioelectrical Impedance Change after Ischemia and Reperfusion Injury in Liver and What it Causes?
Sung Su Yun
Hanyang Med Rev. 2013;33(3):154-159.    doi: 10.7599/hmr.2013.33.3.154.


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