Myocardial reperfusion: Leukocyte accumulation in the ischemic and remote non-ischemic regions

Neutrophil accumulation in the first hour of myocardial reperfusion was ass essed in dog hearts submitted to ischemia with and without necrosis, In ane sthetized dogs, the left anterior descending coronary artery was occluded f or 20 min (group IS-20 n = 7) and for 90 min (group IS-90 n = 6), Immediate ly after reperfusion, Tc-99m-Ceretec (Exametazime-Amersham) labeled neutrop hils were injected into a central vein and 60 min later the dogs were kille d. The left ventricle was isolated, weighed, and sliced. Six sections, 3 fr om normal and 3 from reperfused regions, were divided into endocardial and epicardial layers. Myocardial and blood radiometry were used to evaluate th e neutrophil accumulation during reperfusion. The differences between leukocyte accumulation in both groups were assessed comparing the ischemic/normal relations in the endocardial and epicardial layers. A second comparison considered myocardium/blood relations to allow the evaluation of differences between remote normal myocardial areas of the two experimental groups. In dogs submitted to 20 min of ischemia, leukocytes accumulated significant ly more (P < 0.01) in the reperfused myocardium as compared with the non-is chemic region. The increase occurred both in the endocardial (1.49 +/- 0.20 ) and epicardial (1.48 +/- 0.29) regions, After 90 min ischemia, leukocyte accumulation was more intense and predominant in endocardium where there wa s a 4-fold (3.97 +/- 1.28) increase over the non-ischemic region, while in the epicardium this relation was only 2.5-fold (2.56 +/- 0.98). In the remote non-ischemic myocardium, leukocyte accumulation was greater i n dogs submitted to 90 min of ischemia compared to the 20 min group (P < 0. 01), without distinction between endocardial and epicardial layers, This ac cumulation in territories of non-culprit coronary arteries may be related t o the blood flow abnormalities and matrix structure changes that occur in t hese regions during the development of an acute myocardial infarction and i ts natural repair.