The effect of Dexmedetomidine on remote organ injury in the lung in rats with pancreatic ischemia reperfusion model.

Introduction: Pancreatic ischemia-reperfusion (IR) injury can trigger acute lung injury by causing remote organ involvement. Dexmedetomidine has been reported to exhibit antioxidant and cytoprotective effects in various organs. This study aimed to evaluate the protective effects of dexmedetomidine on lung tissue at the histopathological and biochemical levels in an experimental pancreatic IR model.

Methods: A total of 24 male Wistar-Albino rats were randomly divided into four groups: Sham, Sham + Dexmedetomidine, Ischemia-Reperfusion (IR), and IR + Dexmedetomidine (IR-D). Pancreatic ischemia was induced in the IR and IR-D groups by clamping the inferior splenic and gastroduodenal arteries. In the dexmedetomidine groups, the drug was administered intraperitoneally. Lung tissues were examined using hematoxylin-eosin staining; neutrophil infiltration, alveolar wall thickness, and total injury score were calculated. Levels of thiobarbituric acid reactive substances (TBARS), enzyme activities of catalase, glutathione-S-transferase (GST), and arylesterase were measured as markers of oxidative stress.

Results: The IR group exhibited significantly greater neutrophil infiltration/aggregation compared to the Sham group (p = 0.002) and the Sham + Dexmedetomidine group (p = 0.05). Alveolar wall thickness was significantly increased in the IR group compared to both the Sham and Sham + Dexmedetomidine groups (p < 0.001 for both). The total lung injury score was markedly higher in the IR group than in the Sham and Sham + Dexmedetomidine groups (p < 0.001). In the IR-D group, alveolar wall thickness (p = 0.032) and total injury score (p = 0.037) were significantly reduced compared to the IR group. TBARS levels were significantly elevated in the IR group (p = 0.001), while a significant reduction was observed in the IR-D group (p = 0.025). Catalase and arylesterase activities were lower in both IR and IR-D groups compared to the control, but dexmedetomidine significantly increased catalase (p = 0.045) and arylesterase (p = 0.018) activities compared to the IR group.

Conclusion: Dexmedetomidine significantly reduced oxidative stress, alleviated alveolar structural damage, and decreased the total injury score in lung tissue in a pancreatic IR model. These findings suggest that dexmedetomidine may be a potential pharmacological agent for preventing pulmonary complications that can arise following pancreatic surgery or severe pancreatitis.