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Aprotinin Decreases Ischemic Damage During Coronary Revascularization
Author(s) -
Lazar Harold L.,
Bao Yusheng,
Tanzillo Leslie,
O'Gara Paul,
Reardon Deborah,
Price David,
Crowley Richard,
Cabral Howard J.
Publication year - 2005
Publication title -
journal of cardiac surgery
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.428
H-Index - 58
eISSN - 1540-8191
pISSN - 0886-0440
DOI - 10.1111/j.1540-8191.2005.00136.x
Subject(s) - aprotinin , medicine , cardiology , revascularization , bradykinin , myocardial infarction , anesthesia , coronary occlusion , ischemia , receptor
Background and Aim: This study sought to determine whether the favorable anti‐inflammatory effects of aprotinin might limit ischemic damage during the revascularization of ischemic myocardium. Methods: Twenty pigs underwent 90 minutes of coronary occlusion followed by 45 minutes of blood cardioplegic arrest and 180 minutes of reperfusion. Ten animals received a loading dose of aprotinin (40,000 kallikrein inhibiting units/kg) during the start of coronary occlusion followed by an infusion of 20,000 kallikrein inhibiting units/kg/hour. Ten other animals received no aprotinin. Summary statistics are expressed as the mean ± standard error. Results: The aprotinin‐treated animals required less cardioversions for ventricular arrhythmias (1.0 ± 0.7 vs. 3.6 ± 0.6; p < 0.001), accumulated less lung water (1.0 ± 0.2% change vs. 6.2 ± 0.9% change; p = 0.038), had more complete coronary relaxation to bradykinin (34.1 ± 5.9% change vs. 9.2 ± 3.5% change; p = 0.01), and had reduced infarct size (area necrosis/area risk = 20 ± 1.1% vs. 39 ± 1.2%; p = 0.003). Conclusions: Aprotinin limits ischemic injury during acute coronary revascularization by decreasing ventricular arrhythmias and lung edema, preserving endothelial function, and minimizing myocardial necrosis.