Abstract

Aim: This study aimed to evaluate the effects of dexmedetomidine (Dex), commonly used during the intensive care process—particularly in the postoperative period due to its analgesic and sedative properties— on lower extremity skeletal muscle ischemia–reperfusion injury (IRI) in an experimental ruptured abdominal aortic aneurysm (RAAA) rat model.
Material and Methods: Twenty-four male Sprague Dawley rats (3–4 months old; mean weight 244±32 g) were randomly allocated into three groups: SHAM, IRI, and ischemia–reperfusion injury treated with intraperitoneal 100mcg/kg dexmedetomidine (IRI&Dex). An experimental RAAA model was established in all groups. Lower extremity skeletal muscle tissues were harvested and evaluated using histopathological, immunohistochemical, and biochemical analyses.
Results: Light microscopic examination revealed normal myofibrillar architecture with typical nuclei in the SHAM group, widespread necrotic myofibrils with pyknotic nuclei in the IRI group, and predominantly preserved myofibrillar structures with occasional necrosis in the IRI&Dex group. Immunohistochemical analysis demonstrated dense actin and myosin positivity in the SHAM group, a marked reduction in the IRI group, and a significant increase in the IRI&Dex group compared to the IRI group. Caspase-3 expression was normal in the SHAM group, elevated in the IRI group, and near to normal in the IRI&Dex group. Biochemical analyses showed decreased glutathione (GSH) and increased malondialdehyde (MDA) levels in the IRI group, whereas Dex treatment significantly increased GSH and reduced MDA levels compared to the IRI group.
Conclusion: Histopathological, immunohistochemical, and biochemical findings indicate that dexmedetomidine markedly attenuates ischemia–reperfusion injury in lower extremity skeletal muscle in a rat model of ruptured abdominal aortic aneurysm.

Key words: Ischemia-reperfusion, dexmedetomidine, skeletal muscle