HISTOLOGICAL STUDIES ON POSTISCHEMIC RAT SKELETAL-MUSCLES - WITH EMPHASIS ON THE TIME OF LEUKOCYTE INVASION

Several studies have suggested that the damage after ischemic injuries increases during reperfusion and that this reperfusion damage is medi ated through granulocytes which invade the damaged area. The present s tudy was undertaken to test these hypotheses by histological investiga tions of the anterior tibial muscles in a rat hind limb tourniquet mod el after 4.5 h of complete ischemia and graded periods of reperfusion. Uptake of albumin into damaged muscle fibers was demonstrated immunoh istochemically and used to determine the extent of the ischemic lesion s. The size of the lesions was measured morphometrically on immunostai ned sections from paraffin-embedded material. Granulocytes in and outs ide the capillaries were counted on slides from historesin-embedded ma terial. Generally, there was a compact central area in the muscles whi ch showed necrosis of all fibers and many capillaries, little intersti tial edema, and little or no invasion of granulocytes or macrophages. The central core did not increase in size during the postoperative per iod. Outside this are there was a zone of partial tissue destruction w ith quite marked interstitial edema. This zone also remained unchanged in size but it is uncertain whether the number of necrotic fibers inc reased with time. There was an increasing invasion of granulocytes in this outer zone from 5 to 24 h after release of the occlusion and mono cyte/macrophage invasion was seen from 48 h. Outside this zone there w as a subfacial zone with normal muscle fibers in all cases. It is conc luded that the central area of complete tissue destruction was present at the time of release of the occlusion and did not increase in size during the further postoperative course. There was no indication that granulocytes participated in this damage. The extent of the partially damaged area also remained unchanged during the postoperative course. It is conceivable that granulocytes aggravated the lesions by increasi ng the number of necrotic fibers in this peripheral area but not befor e 5 h after release of the occlusion. This is later than described in previous studies.