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Updated: Jul 8, 2026
Isolation of Macrophage Subsets and Stromal Cells from Human and Mouse Myocardial Specimens
Published on: December 17, 2019
Are macrophages involved in early myocardial reperfusion injury?
L Formigli1, L I Manneschi, C Nediani
1Department of Anatomy, University of Florence, Italy.
Background:
Neutrophils are the predominant phagocytes in the early stages of myocardial ischemia-reperfusion response and are also implicated in the development of tissue damage. This study examined the role of recruited macrophages in the evolution of this tissue injury.
Methods:
Farm pigs were subjected to 30 minutes of myocardial ischemia followed by 30 minutes of reperfusion. Biopsy samples were taken from the control, ischemic, and ischemic-reperfused left ventricle wall and processed for both morphologic and biochemical analyses. In situ production of tumor necrosis factor-alpha was evaluated by Western blot and immunofluorescence. A full hemodynamic evaluation was also performed.
Results:
Myocardial ischemia and early reperfusion caused marked neutrophil and macrophage tissue accumulation and tumor necrosis factor-alpha production by the injured tissue. Immunofluorescence studies allowed us to localize tumor necrosis factor-alpha predominantly in tissue-infiltrating macrophages. No depression in the global myocardial contractile function was observed, either during ischemia or after reperfusion.
Conclusions:
These data suggest that the newly recruited macrophages within the ischemic and early post-ischemic myocardium may play a role in promoting neutrophil tissue infiltration and subsequent neutrophil-induced tissue dysfunction by producing tumor necrosis factor-alpha.
Insights
Macrophages recruited to the heart after ischemia-reperfusion injury produce tumor necrosis factor-alpha. This promotes neutrophil infiltration, potentially worsening myocardial tissue damage.
Area of Science:
- Cardiovascular Research
- Immunology
- Myocardial Infarction
Background:
- Neutrophils are key phagocytes in early myocardial ischemia-reperfusion.
- Neutrophils contribute to tissue damage during this process.
- The role of macrophages in this injury evolution requires further investigation.
Purpose of the Study:
- To investigate the role of recruited macrophages in myocardial ischemia-reperfusion injury.
- To assess the contribution of macrophages to tissue damage and inflammatory responses.
Main Methods:
- Pigs underwent 30 minutes of myocardial ischemia followed by 30 minutes of reperfusion.
- Biopsy samples were analyzed morphologically and biochemically.
- In situ tumor necrosis factor-alpha production was evaluated using Western blot and immunofluorescence.
Main Results:
- Myocardial ischemia and reperfusion led to significant neutrophil and macrophage accumulation.
- Tumor necrosis factor-alpha was produced by injured tissue, primarily localized in macrophages.
- No depression in global myocardial contractile function was observed during or after ischemia-reperfusion.
Conclusions:
- Recruited macrophages in the ischemic myocardium produce tumor necrosis factor-alpha.
- This macrophage-derived tumor necrosis factor-alpha may promote neutrophil infiltration.
- This process could contribute to neutrophil-induced myocardial dysfunction.
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