title: Histological studies on postischemic rat skeletal muscles. With emphasis on the time of leukocyte invasion.
abstract: Several studies have suggested that the damage after ischemic injuries increases during reperfusion and that this reperfusion damage is mediated through granulocytes which invade the damaged area. The present study was undertaken to test these hypotheses by histological investigations of the anterior tibial muscles in a rat hind limb tourniquet model after 4.5 h of complete ischemia and graded periods of reperfusion. Uptake of albumin into damaged muscle fibers was demonstrated immunohistochemically and used to determine the extent of the ischemic lesions. The size of the lesions was measured morphometrically on immunostained sections from paraffin-embedded material. Granulocytes in and outside the capillaries were counted on slides from historesin-embedded material. Generally, there was a compact central area in the muscles which showed necrosis of all fibers and many capillaries, little interstitial edema, and little or no invasion of granulocytes or macrophages. The central core did not increase in size during the postoperative period. Outside this are there was a zone of partial tissue destruction with quite marked interstitial edema. This zone also remained unchanged in size but it is uncertain whether the number of necrotic fibers increased with time. There was an increasing invasion of granulocytes in this outer zone from 5 to 24 h after release of the occlusion and monocyte/macrophage invasion was seen from 48 h. Outside this zone there was a subfacial zone with normal muscle fibers in all cases. It is concluded 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 increasing the number of necrotic fibers in this peripheral area but not before 5 h after release of the occlusion. This is later than described in previous studies.
authors.affiliation: Institute for Surgical Research, National Hospital, Oslo, Norway.
authors.forename: S
authors.initials: S
authors.lastname: Skjeldal
authors.forename: A
authors.initials: A
authors.lastname: Torvik
authors.forename: B
authors.initials: B
authors.lastname: Grøgaard
authors.forename: L
authors.initials: L
authors.lastname: Nordsletten
authors.forename: T
authors.initials: T
authors.lastname: Lyberg
mesh_terms: D000818:Animals; D004195:Disease Models, Animal; D006098:Granulocytes / Q000473:pathology; D007962:Leukocytes / Q000473:pathology*; D008264:Macrophages / Q000473:pathology; D008297:Male; D009000:Monocytes / Q000473:pathology; D009132:Muscles / Q000098:blood supply / Q000293:injuries / Q000473:pathology*; D009336:Necrosis; D051381:Rats; D017208:Rats, Wistar; D015427:Reperfusion Injury / Q000473:pathology*