Evidence for Plasma-Mediated Neutrophil Superoxide Anion Production during Myocardial Infarction

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Abstract
The participation of polymorphonuclear neutrophils (PMN) in the development of free-oxygen-mediated myocardial injury is well documented, but direct evidence that PMN-oriented stimuli released to the peripheral blood are able to stimulate PMN free oxygen radical production is missing. We have previously reported that peripheral blood plasma obtained from patients with acute myocardial infarction has chemotactic activity for neutrophils and augments PMN adherence. To investigate whether neutrophilic stimuli released to peripheral blood may induce PMN superoxide anion (O-2 production, we incubated PMN from healthy donors with plasma from patients with acute transmural infarction. PMN O-2 production was measured by cytochrome c reduction. PMN O-2 was higher under the influence of plasma obtained on the day of admission (24.66 ± 12.41) and 1 day after onset of acute ischemia (22.91 ± 10.37) as compared with those observed after incubation with saline (4.18 ± 1.37; negative control) or zymosan-activated plasma (11.07 ± 3.4; activated complement cascade positive control). In the following days, plasma-mediated PMN O-2 decreased: 13.27 ± 1.96; 12.37 ± 3.54 and 8.18 ± 1.56 after incubation with plasma obtained 2, 3 and 7 days after onset of symptoms, respectively. The results indicate an additional possibility of monitoring the inflammatory response to myocardial necrosis.

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