The purposes of this investigation were (1) to develop an in vivo method of determining the myocardium at risk after experimental
coronary occlusion; (2) to define the spatial geometry of the salvageable ischemic border zone;
an (3) to assess the ability of
flurbiprofen, an
antiinflammatory agent, to protect ischemic myocardium from
necrosis. Twenty-two open-chest dogs underwent left anterior descending coronary artery occlusion and were randomized to treated (
flurbiprofen 1 mg/kg i.v. at 30 minutes and 4 hours after occlusion; n = 11) or control (saline; n = 11) groups. Six hours after occlusion,
methylene blue, 3 ml/lg, was injected into the left atrium, and immediately thereafter the hearts were removed and sliced transversely. Areas not perfused by
methylene blue (area at risk [Ar]) were traced, planimetered, and compared to the area of
necrosis (An) after incubation in
triphenyltetrazolium chloride. The Ar for the two groups were similar (control 28.2 +/- 2.6%; treated 25.2 +/- 2.3% of total left ventricle; NS). In control dogs, An/Ar was 96.2 +/- 0.7%, with similar values for the epicardium and endocardium. In treated dogs, An/Ar was 66.9 +/- 8.9% (p < 0.001), with greater epicardial than endocardial salvage. Topographic superimposition of the An on the Ar showed that salvage occurred both on the epicardial and lateral aspects of the
infarct. We conclude that (1) the in vivo
methylene blue method of assessing myocardium at risk is useful in standardizing experimental
infarct size; (2)
flurbiprofen, administered 30 minutes and 4 hours after occlusion, is a potent agent for reducing
infarct size; and (3) salvage of myocardium occurs both at the lateral and epicardial borders of the
infarct in dogs treated with
flurbiprofen.