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Polymorphonuclear leucocytes increase reperfusion injury in skeletal muscle
S Oredsson1, P Qvarfordt, G Plate
1Department of Surgery, Helsingborg Hospital, Lund University, Sweden.
Summary
Polymorphonuclear leucocytes (PMNLs) contribute to skeletal muscle reperfusion injury. Free radical scavengers mitigate PMNL-induced damage, indicating a role for oxygen-derived free radicals in this process.
Area of Science:
- Biomedical Science
- Surgical Research
- Physiology
Background:
- Reperfusion injury is a significant complication following ischemia.
- Polymorphonuclear leucocytes (PMNLs) are implicated in inflammatory processes.
- Oxygen-derived free radicals play a role in cellular damage.
Purpose of the Study:
- To investigate the impact of PMNLs on skeletal muscle reperfusion injury in rabbits.
- To determine the involvement of oxygen-derived free radicals in PMNL-mediated injury.
Main Methods:
- An isolated rabbit limb perfusion model was utilized.
- Hindlimbs underwent 4 hours of ischemia followed by 2 hours of reperfusion.
- PMNLs, with or without free radical scavengers (SOD and catalase), were added to the reperfusion buffer.
Main Results:
- PMNLs significantly increased myeloperoxidase (MPO) activity and [Tc99]methylenediphosphonate (MDP) uptake, indicating PMNL accumulation and muscle necrosis.
- Treatment with SOD and catalase reduced MPO activity, MDP uptake, and muscle water content (MWC).
- PMNLs exacerbated histological signs of reperfusion injury.
Conclusions:
- PMNLs partially mediate skeletal muscle reperfusion injury.
- Free radical scavengers effectively reduce PMNL-dependent injury and PMNL accumulation.
- Oxygen-derived free radicals are key mediators in PMNL-dependent reperfusion injury and PMNL-endothelial interactions.