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Updated: May 25, 2026

Organ Ischemia-Reperfusion Injury by Simulating Hemodynamic Changes in Rat Liver Transplant Model
Published on: March 6, 2021
Systemic lidocaine does not attenuate hepatic dysfunction after liver surgery in rats
Wilmar de Graaf1, Gwen M P Diepenhorst, Susanne Herroeder
1Department of Surgery, Academic Medical Center, Amsterdam, Amsterdam, The Netherlands.
Systemic lidocaine did not protect against liver injury from ischemia-reperfusion (I/R) in rats. The drug did not reduce liver damage or improve liver function following I/R, despite its known effects in other organs.
Area of Science:
- Hepatology and Surgical Research
- Pharmacology and Toxicology
Background:
- Ischemia-reperfusion (I/R) injury is a significant risk in liver surgery, potentially leading to liver dysfunction or failure.
- Lidocaine has demonstrated protective effects against I/R injury in the heart, lung, and brain, possibly by modulating inflammation and apoptosis.
- The study aimed to investigate lidocaine's efficacy in mitigating hepatocellular damage and improving liver function in hepatic I/R injury.
Purpose of the Study:
- To evaluate the protective effects of systemic lidocaine on hepatocellular damage and liver function in a rat model of hepatic I/R injury.
- To explore the underlying mechanisms, including inflammatory responses and apoptosis, associated with lidocaine's potential therapeutic action.
Main Methods:
- Two standardized rat models of hepatic I/R injury were utilized, including a 70% I/R model and a model combining ischemia with partial hepatectomy.
- Systemic lidocaine was administered continuously from 30 minutes pre-ischemia to 20 minutes post-reperfusion.
- Hepatocellular function, inflammation (leukocyte influx), and apoptosis were assessed using biochemical, histological, and molecular assays.
Main Results:
- Hepatic I/R injury significantly increased hepatocellular damage in both models.
- No significant differences in hepatocellular damage or postoperative liver function were observed between control and lidocaine-treated groups.
- Lidocaine administration did not alter I/R-induced leukocyte influx, indicating no significant anti-inflammatory effect in the liver.
Conclusions:
- Systemic lidocaine, at therapeutic concentrations, did not attenuate hepatocellular damage following hepatic I/R injury.
- Lidocaine treatment failed to improve postoperative liver function in the studied models.
- The findings suggest that lidocaine may not be an effective therapeutic agent for preventing or treating hepatic I/R injury.
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