J Korean Surg Soc.  2010 Jun;78(6):390-397. 10.4174/jkss.2010.78.6.390.

Impaired Cation Transport May Lead to Bioelectrical Impedance Changes during Hepatic Ischemia

Affiliations
  • 1Research Institute of Biomedical Engineering, College of Medicine, Yeungnam University, Daegu, Korea. ssyun@med.yu.ac.kr
  • 2Department of Physiology, College of Medicine, Yeungnam University, Daegu, Korea.
  • 3Department of Surgery, College of Medicine, Yeungnam University, Daegu, Korea.

Abstract

PURPOSE
Ischemia and reperfusion (I/R) injury is a major cause of hepatic failure after liver surgery, but there is no direct method to monitor it in real-time (like an electrocardiogram in heart disease) during surgery. Recently we found the possible role of bioelectrical impedance (BEI) to monitor I/R injury in liver. But the mechanism responsible for ischemia-related BEI changes has not been clearly determined.
METHODS
The authors used an LCR meter to quantify BEI changes at 0.12 KHz. Livers were subjected to 70% partial ischemia for 120 minutes, and ATP contents, cation changes in extracellular fluid (ECF; determined using an in vivo intracellular microdialysis technique), hepatocyte sizes, and histological changes were then examined.
RESULTS
Liver tissue BEI was found to increase gradually during the first 60 minutes of ischemia and then tended to plateau. During the same period, intracellular ATP contents decreased to below 20% of the baseline level, [Na+] in ECF decreased from 150.4+/-3.8 to 97.8+/-10.6 mmol/L, and [K+] in ECF increased from 7.5+/-0.3 to 34.3+/-5.5 mmol/L during the first 60 minutes of ischemia. Hepatocyte diameter increased by ~20% during the first 60 minutes of ischemia.
CONCLUSION
This study suggests that BEI changes during hepatic ischemia are probably caused by sodium and potassium concentration changes in the ECF due to reduced intracellular ATP contents.

Keyword

Ischemia; Bioelectrical impedance; Liver; Microdialysis; Cation

MeSH Terms

Adenosine Triphosphate
Electric Impedance
Electrocardiography
Extracellular Fluid
Heart
Hepatocytes
Ischemia
Liver
Liver Failure
Microdialysis
Organothiophosphorus Compounds
Potassium
Reperfusion
Sodium
Adenosine Triphosphate
Organothiophosphorus Compounds
Potassium
Sodium

Figure

  • Fig. 1 Bioelectrical impedance changes in liver tissue during 120 minutes of ischemia.

  • Fig. 2 ATP contents of the liver during 120 minutes of ischemia. *P<0.05 vs 0 minutes (non-ischemia).

  • Fig. 3 Zero net flux curves for [Na+] and [K+] in Hartmann's solution. Points 1 to 4 show differences between dialysate and perfusate after perfusing 4 known different perfusates. Concentrations of [Na+] and [K+] in perfusates 1 to 4 were 0, 75, 150, 225 mM for Na+ and 0, 5, 10, 15 mM for K+, respectively.

  • Fig. 4 Zero net flux curves for [Na+] and [K+] in liver tissue ECF in vivo prior to ischemia. Points 1 to 4 show differences between dialysate and perfusate after perfusing 4 known different perfusates. Concentrations of [Na+] and [K+] in perfusates 1 to 4 were 0, 75, 150, 225 mM for Na+ and 0, 5, 10, 15 mM for K+, respectively.

  • Fig. 5 Changes in ECF [Na+] and [K+] in liver tissues in vivo during 120 minutes of ischemia. *P<0.05 vs 0 minutes (non-ischemia).

  • Fig. 6 The correlation between BEI and summed [Na+] and [K+] in liver tissue ECF in vivo.

  • Fig. 7 Changes in hepatocyte diameter during 120 minutes of ischemia. *P<0.05 vs 0 minutes (non-ischemia).


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