Abstract
The aim of this study was to examine whether dexmedetomidine improves acute liver injury in a rat model. Twenty-eight male Wistar albino rats weighing 300–350 g were allocated randomly to four groups. In group 1, normal saline (NS) was injected into the lungs and rats were allowed to breathe spontaneously. In group 2, rats received standard ventilation (SV) in addition to NS. In group 3, hydrochloric acid was injected into the lungs and rats received SV. In group 4, rats received SV and 100 µg/kg intraperitoneal dexmedetomidine before intratracheal HCl instillation. Blood samples and liver tissue specimens were examined by biochemical, histopathological, and immunohistochemical methods. Acute lung injury (ALI) was found to be associated with increased malondialdehyde (MDA), total oxidant activity (TOA), oxidative stress index (OSI), and decreased total antioxidant capacity (TAC). Significantly decreased MDA, TOA, and OSI levels and significantly increased TAC levels were found with dexmedetomidine injection in group 4 (P < 0.05). The highest histologic injury scores were detected in group 3. Enhanced hepatic vascular endothelial growth factor (VEGF) expression and reduced CD68 expression were found in dexmedetomidine group compared with the group 3. In conclusion, the presented data provide the first evidence that dexmedetomidine has a protective effect on experimental liver injury induced by ALI.
Highlights
Acute lung injury (ALI) is a condition that contributes to morbidity and mortality in critically ill patients [1]
We found significantly lower pH and PaO2 in group 3 compared with the control group (P = 0.002 and P = 0.001, respectively; Table 1), while the PaCO2 value of group 3 was significantly higher than that of the control group (P < 0.001; Table 1)
Liver injury may be caused by acute hypoxemia, a lifethreatening event associated with high morbidity and mortality [6, 28]
Summary
Acute lung injury (ALI) is a condition that contributes to morbidity and mortality in critically ill patients [1]. Because pharmacological agents have poor benefit in ALI treatment, the mortality rate is still high [4]. This condition induces a systemic response and causes the release of harmful substances that may affect remote organs such as the liver by causing hypoxemia. Acute hypoxemia is the main cause of liver injury in ALI. Respiratory failure leads to liver hypoxia by several hemodynamic mechanisms [6]. Systemic hypoxemia is the essential factor that represents a potential role for development of liver injury in respiratory failure [7]. Hypoxia may activate NADPH oxidase in Kupffer cells and xanthine oxidase in hepatocytes and these can lead to hepatic injury [8]
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