Hanyang Med Rev.  2013 Aug;33(3):154-159. 10.7599/hmr.2013.33.3.154.

Significance of Bioelectrical Impedance Change after Ischemia and Reperfusion Injury in Liver and What it Causes?

• Yun SS

• KMID: 2168258
• DOI: http://doi.org/10.7599/hmr.2013.33.3.154

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 ECG 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 a LCR meter to quantify BEI changes at 0.12 KHz. Livers were subjected to 70% partial ischemia for 120 minutes, and ATP content, 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 content 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 approximately 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 content.

Keyword

Electric Impedance; Adenosine Triphosphate; Liver; Microdialysis; Cations

MeSH Terms

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

Figure

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  Fig. 1 Changes of bioelectrical impedance in liver during ischemia according to frequency 120 Hz to 100 KHz (n=5). Ref. 20 with permission from the Korean Association of Hepato-Biliary and Pancreas Surgery.

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  Fig. 2 Change of bioelectrical impedance in liver during 30 minutes ischemia and 20 minutes reperfusion at 120 Hz. Bars represent means values±SD (n=5). Ref. 20 with permission from the Korean Association of Hepato-Biliary and Pancreas Surgery.

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  Fig. 3 Change of bioelectrical impedance in liver during 120 minutes ischemia. Bars represent means values±SD (n=5). Ref. 20 with permission from the Korean Association of Hepato-Biliary and Pancreas Surgery.

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  Fig. 4 ATP content of the ischemic liver at 30 minutes interval during 120 minutes ischemia. Ref. 22 with permission from Korean Surgical Society.

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  Fig. 5 Palmitic acid oxidation rate of the ischemic liver at 30 minutes interval during 120 minutes ischemia. Ref. 22 with permission from Korean Surgical Society.

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  Fig. 6 Microscopic findings of the ischemic liver during 120 minutes ischemia. Ref. 22 with permission from Korean Surgical Society. (A, C, E, G, I) hematoxylin eosin (H&E) stain×40, (B, D, F, H, J) TUNEL stain×40. (A, B) control, (C, D) 30 minutes ischemia, (E, F) 60 minutes ischemia, (G, H) 90 minutes ischemia, (I, J) 120 minutes ischemia.

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  Fig. 7 Changes in hepatocyte diameter during 120 minutes of ischemia. *P<0.05 vs 0 minutes (non-ischemia). Ref. 14 with permission from Korean Surgical Society.

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  Fig. 8 Changes in ECF [Na+] and [K+] in liver tissues in vivo during 120 minutes of ischemia. *P<0.05 vs 0 minutes (non-ischemia). Ref. 14 with permission from Korean Surgical Society.

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  Fig. 9 The correlation between BEI and summed [Na+] and [K+] in liver tissue ECF in vivo. Ref. 14 with permission from Korean Surgical Society.

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