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Neutrophil-induced myocardial cell damage and active oxygen metabolites
1First Department of Medicine, Osaka University School of Medicine, Japan.
Abstract:
Free radicals derived from polymorphonuclear leukocytes (PMN) have been suggested to play an important role in myocardial ischemia-reperfusion injury. To define the mechanism by which activated PMN exacerbate ischemic myocardial damage, we investigated the extent of cell injury, free radical generation and lipid peroxidation in embryo mouse myocardial cells co-incubated with activated PMN. The generation of free radicals derived from PMN correlated with the extent of myocardial cell injury. Among the cell sheets preconditioned with hypoxic and glucose free medium, PMN-adhered myocardial cells were initially injured after adding PMN activator, extending to adjacent cells. Chemiluminescence emission and thiobarbituric acid reactive substance in the co-incubated cells were markedly increased and sustained compared with those in each cell monoincubation. The augmented lipid peroxidation was related to the progression of myocardial cell injury. These results indicate that PMN-derived free radicals cause membrane disruption, contributing to the progression of myocardial injury.
Insights
Free radicals from white blood cells (polymorphonuclear leukocytes, PMN) worsen heart damage after blood flow is restored. These PMN-derived free radicals cause cell membrane damage, increasing injury progression.
Area of Science:
- Cardiovascular Research
- Cell Biology
- Immunology
Background:
- Polymorphonuclear leukocytes (PMN) are implicated in myocardial ischemia-reperfusion injury.
- The precise mechanism of PMN-exacerbated ischemic myocardial damage requires further elucidation.
Purpose of the Study:
- To investigate the role of PMN-derived free radicals in myocardial cell injury.
- To determine the relationship between PMN activation, free radical generation, lipid peroxidation, and myocardial cell damage.
Main Methods:
- Co-incubation of embryo mouse myocardial cells with activated PMN.
- Measurement of cell injury, free radical generation (chemiluminescence), and lipid peroxidation (thiobarbituric acid reactive substance).
- Assessment of PMN adherence and activation on myocardial cell sheets under hypoxic conditions.
Main Results:
- PMN-derived free radical generation strongly correlated with the extent of myocardial cell injury.
- PMN activation led to injury of adhered myocardial cells and adjacent cells.
- Co-incubation significantly increased and sustained chemiluminescence and thiobarbituric acid reactive substance levels, indicating augmented free radical production and lipid peroxidation.
- Increased lipid peroxidation was directly related to the progression of myocardial cell injury.
Conclusions:
- PMN-derived free radicals are a key factor in exacerbating myocardial ischemia-reperfusion injury.
- These free radicals induce membrane disruption in myocardial cells, contributing to progressive injury.
- Targeting PMN-derived free radicals may offer a therapeutic strategy for reducing myocardial damage.