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Effects of ischemic postconditioning on expressions of pentraxin-related protein 3 and neutrophil CD11b in the plasma of patients with acute myocardial infarction after percutaneous coronary intervention
OBJECTIVE: To evaluate the effects of ischemic postconditioning on expressions of pentraxin-related protein 3 (PTX3) and neutrophil CD11b in the plasma of patients with acute myocardial infarction (AMI) after percutaneous coronary intervention (PCI). METHODS: Fifty-six patients who had AMI with ST-s...
Autores principales: | , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Professional Medical Publications
2016
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4859037/ https://www.ncbi.nlm.nih.gov/pubmed/27182254 http://dx.doi.org/10.12669/pjms.322.9457 |
Sumario: | OBJECTIVE: To evaluate the effects of ischemic postconditioning on expressions of pentraxin-related protein 3 (PTX3) and neutrophil CD11b in the plasma of patients with acute myocardial infarction (AMI) after percutaneous coronary intervention (PCI). METHODS: Fifty-six patients who had AMI with ST-segment elevation were randomly divided into a control group and an ischemic postconditioning group (n=28). Both groups received emergency PCI. After recanalization of infarct-related arteries, the control group did not receive intervention within three minutes, while the ischemic postconditioning group was treated by low-pressure filling and emptying of balloon within one minute. The plasma expressions of PTX3 before and 24 hour after PCI were detected by ELISA, and those of neutrophil CD11b were detected by flow cytometry. RESULTS: PTX3 and neutrophil CD11b expressions of the two groups were similar before PCI, but those of the ischemic postconditioning group significantly decreased 24 hour after PCI (P<0.05). CONCLUSION: Ischemic postconditioning lowered the expressions of PTX3 and neutrophil CD11b in AMI patients after PCI, inhibited inflammatory response, reduced the adhesion between leukocytes and endothelial cells, and protected the ischemic-reperfused myocardium. |
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