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

Neutrophil accumulation in the first hour of myocardial reperfusion was assessed in dog hearts submitted to ischemia with and without necrosis. In anesthetized dogs, the left anterior descending coronary artery was occluded for 20 min (group IS-20 n = 7) and for 90 min (group IS-90 n = 6). Immediately after reperfusion, 99m Tc-Ceretec (Exametazime-Amersham) labeled neutrophils were injected into a central vein and 60 min later the dogs were killed. The left ventricle was isolated, weighed, and sliced. Six sections, 3 from normal and 3 from reperfused regions, were divided into endocardial and epicardial layers. Myocardial and blood radiometry were used to evaluate the 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 significantly more (P < 0.01) in the reperfused myocardium as compared with the non-ischemic 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 was 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 in dogs submitted to 90 min of ischemia compared to the 20 min group (P < 0.01), without distinction between endocardial and epicardial layers. This accumulation in territories of non-culprit coronary arteries may be related to the blood flow abnormalities and matrix structure changes that occur in these regions during the development of an acute myocardial infarction and its natural repair.