Key result
Acute MI links to transient neutrophil exhaustion and reduced superoxide generation that normalizes by day 7.
Observational
Circulating neutrophils isolated from patients 3–4 h after a myocardial infarction produced less {article}{empty}{document}O · 2{document} compared with controls, when stimulated with phorbol myrystate acetate or formyl‐methionine‐leucine‐phenylalanine. Three days after the infraction the {article}{empty}{document}O · 2{document} generation elicited by both stimuli further decreased markedly. Seven and 15 days after infarction the {article}{empty}{document}O · 2{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 {article}{empty}{document}O · 2{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.
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Guarnieri et al. (1990) conducted an observational in Myocardial infarction. Myocardial infarction (with ex vivo neutrophil stimulation by PMA or fMLP) vs. Controls was evaluated on Superoxide anion (O2.-) generation by isolated circulating neutrophils. Circulating neutrophils isolated 3-4 h and 3 days after myocardial infarction showed markedly reduced superoxide generation and cellular exhaustion vs controls, normalizing by days 7-15.
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