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Reduced oxidative activity of circulating neutrophils in patients after myocardial infarction
Author(s) -
Guarnieri Carlo,
Melandri Giovanni,
Caldarera Ilaria,
Scheda Mauro,
Ligabue Amedeo,
Guizzardi Sandro,
Branzi Angelo
Publication year - 1990
Publication title -
cell biochemistry and function
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.933
H-Index - 61
eISSN - 1099-0844
pISSN - 0263-6484
DOI - 10.1002/cbf.290080305
Subject(s) - myocardial infarction , medicine , infarction , phorbol , endocrinology , oxidative stress , methionine , chemistry , biochemistry , protein kinase c , phosphorylation , amino acid
Circulating neutrophils isolated from patients 3–4 h after a myocardial infarction produced less \documentclass{article}\pagestyle{empty}\begin{document}$ {\rm O}\frac{ \cdot }{{\rm 2}} $\end{document} compared with controls, when stimulated with phorbol myrystate acetate or formyl‐methionine‐leucine‐phenylalanine. Three days after the infraction the \documentclass{article}\pagestyle{empty}\begin{document}$ {\rm O}\frac{ \cdot }{{\rm 2}} $\end{document} generation elicited by both stimuli further decreased markedly. Seven and 15 days after infarction the \documentclass{article}\pagestyle{empty}\begin{document}$ {\rm O}\frac{ \cdot }{{\rm 2}} $\end{document} stimulated production was only slightly lower than or similar to the control values. The neutrophils of infarcted patients showed an augmented latency period before \documentclass{article}\pagestyle{empty}\begin{document}$ {\rm O}\frac{ \cdot }{{\rm 2}} $\end{document} production compared with controls in response to exogenous stimuli, particularly three days after infarction. Electron microscopy revealed that the neutrophils isolated from the infarcted patients displayed signs of cell exhaustion with few alterations of the plasma membranes when stimulated with phorbol ester. In contrast, control neutrophils displayed alterations of the plasma membranes characteristic of active neutrophils. The results of this study indicate that the circulating neutrophils appear exhausted and functionally inhibited immediately after myocardial infarction.