Significance of Bioelectrical Impedance Change after Ischemia and Reperfusion Injury in Liver and What it Causes?.
10.7599/hmr.2013.33.3.154
- Author:
Sung Su YUN
1
Author Information
1. Department of Surgery, Yeungnam University College of Medicine, Daegu, Korea. ssyun@med.yu.ac.kr
- Publication Type:Review
- Keywords:
Electric Impedance;
Adenosine Triphosphate;
Liver;
Microdialysis;
Cations
- MeSH:
Adenosine Triphosphate;
Cations;
Electric Impedance;
Electrocardiography;
Extracellular Fluid;
Heart;
Hepatocytes;
Ischemia;
Liver;
Liver Failure;
Microdialysis;
Organothiophosphorus Compounds;
Potassium;
Reperfusion;
Reperfusion Injury;
Sodium
- From:Hanyang Medical Reviews
2013;33(3):154-159
- CountryRepublic of Korea
- Language:Korean
-
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.
