Key result
Ibuprofen significantly reduces acute myocardial ischemic damage across 3 of 4 key markers.
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Ibuprofen, a nonsteriodal anti-inflammatory agent, was studied in the early stages of myocardial ischemia in order to determine whether it helps preserve myocardial integrity. Ibuprofen was administered intravenously at a dose of 12.5 mg/kg at the time of coronary artery occlusion and again 2.5 h later. Ibuprofen significantly prevented the loss of myocardial creatine phosphokinase (CPK) release in ischemic cardiac tissue. In addition, this drug significantly returned S-T segment elevation toward normal values, and significantly prevented the myocardial loss of compounds having free amino nitrogen groups, an index of proteolysis. Although ibuprofen moderated the increased plasma CPK activity, plasma CPK values 5 h after coronary occlusion were above control values. Thus, ibuprofen significantly prevented alterations in three of the four indices used to assess myocardial ischemic damage. The protective mechanism of ibuprofen may be via stabilization of cellular membranes (i.e., lysosomal membranes) and to a lesser extent on reduction in myocardial oxygen demand.
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Lefer et al. (2008) studied Acute myocardial ischemia. Ibuprofen vs. Control was evaluated on Myocardial ischemic damage assessed by myocardial CPK loss, S-T segment elevation, myocardial loss of free amino nitrogen groups, and plasma CPK activity. Ibuprofen prevented alterations in 3 of 4 indices of acute myocardial ischemic damage, including myocardial CPK loss and S-T segment elevation.
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