Circulation, Vol 66, 1002-1011, Copyright © 1982 by American Heart Association
JL Romson, BG Hook, VH Rigot, MA Schork, DP Swanson and BR Lucchesi
To assess the ability of ibuprofen to influence the extent of platelet
aggregation and leukocyte infiltration during acute myocardial infarction,
autologous indium-111 (111-In)-labeled platelets or leukocytes were
injected before 60 minutes of left circumflex coronary artery (LCx)
occlusion, followed by 24 hours of reperfusion in the canine heart.
Myocardial infarct size, as a percent of the area at risk, was reduced in
the ibuprofen-treated group (12.5 mg/kg i.v. every 4 hours beginning 30
minutes before LCx occlusion) by 40%, from 48 +/- 4% in control animals to
29 +/- 4% in ibuprofen-treated dogs (p = 0.005). Quantification of the
platelet-associated 111In radioactivity in irreversibly injured myocardium
indicated that ibuprofen did not alter the accumulation of platelets in
infarcted myocardium. In contrast, leukocyte accumulation in infarcted
tissue was reduced significantly. In tissue samples with 0.41-0.60 gram
infarct, the infarcted/normal ratio of leukocyte radioactivity was 12 +/- 2
in control dogs and 4 +/- 1 in ibuprofen-treated dogs, which represents a
67% reduction in leukocyte accumulation in ibuprofen-treated compared with
control dogs. Similar reductions were found in other gram-infarct- weight
categories. Although both platelets and leukocytes accumulate in infarcted
canine myocardium, ibuprofen may exert its beneficial effect on ischemic
myocardium by suppressing the inflammatory response associated with
myocardial ischemia and infarction.
ARTICLES
The effect of ibuprofen on accumulation of indium-111-labeled platelets and leukocytes in experimental myocardial infarction
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