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Circulation, Vol 67, 1016-1023, Copyright © 1983 by American Heart Association
JL Romson, BG Hook, SL Kunkel, GD Abrams, MA Schork and BR Lucchesi
Accumulation of polymorphonuclear neutrophils during the acute inflammatory
response may exacerbate tissue injury through the release of activated
oxygen products or proteolytic enzymes or both. To assess the role of
neutrophils in acute myocardial infarction, circulating neutrophil levels
in dogs were reduced by 77 +/- 2% (mean +/- SEM) by administering rabbit
antiserum to dog neutrophils. Acute myocardial infarction was induced in
open-chest anesthetized dogs by 90 minutes of left circumflex coronary
artery occlusion followed by 6 hours of reperfusion. Dogs treated with
neutrophil antiserum (n = 8) developed myocardial infarcts that were an
average of 43% smaller than infarcts in dogs treated with nonimmune rabbit
serum (n = 7) (27.0 +/- 4.5% vs 47.1% +/- 7.5% of the area at risk, p less
than 0.05). In a saline- treated control group (n = 8), infarct size was
48.0 +/- 4.7% of the area at risk, a value not significantly different from
that of the nonimmune serum group but significantly greater than that in
the neutrophil antiserum dogs (p less than 0.05). There were no major
hemodynamic differences between groups. Histopathologic examination
revealed that infarcted myocardium from dogs given saline or treated with
nonimmune serum had a substantial neutrophilic infiltrate, which was
virtually absent in infarcted tissue from dogs treated with neutrophil
antiserum. These observations suggest that neutrophil accumulation in
response to myocardial ischemia may be responsible for a substantial
portion of the irreversible myocardial injury resulting from temporary
coronary artery occlusion.
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