{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,21]],"date-time":"2026-10-21T18:18:02Z","timestamp":1792606682170,"version":"4.5.0"},"reference-count":55,"publisher":"Wiley","issue":"5","license":[{"start":{"date-parts":[[2005,2,18]],"date-time":"2005-02-18T00:00:00Z","timestamp":1108684800000},"content-version":"vor","delay-in-days":1997,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Journal Orthopaedic Research"],"published-print":{"date-parts":[[1999,9]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p>Major loss of tissue is an almost invariable consequence of severe closed soft\u2010tissue injury. Clinically, the extent of soft\u2010tissue trauma determines the outcome of complex injuries and significantly influences bone healing. With use of a new animal model, this study quantitatively analyzed microcirculation, i.e., nutritive perfusion and leukocyte\u2010endothelial cell interaction, in skeletal muscle after standardized closed soft\u2010tissue injury. By means of a computer\u2010assisted controlled\u2010impact technique, a severe standardized closed soft\u2010tissue injury was induced in the left hindlimb of 28 rats. The rats were assigned to four experimental groups (n = 7 per group) that differed by time of analysis (1.5, 24, 72, and 120 hours after injury); rats that were not injured served as controls (n = 7). Intramuscular pressure was measured, and microcirculation in the rat extensor digitorum longus muscle was analyzed by <jats:italic>in vivo<\/jats:italic> fluorescence microscopy, which allowed assessment of microvascular diameters, functional capillary density, number of rolling and adherent leukocytes in venules, and microvascular permeability. Edema weight gain was quantified by the ratio of wet to dry weight of the extensor digitorum longus muscle. Microvascular perfusion of the skeletal muscle was characterized by a significant reduction in functional capillary density, which was paralleled by an increase in capillary diameter throughout the 120 hours of observation when compared with the controls. Traumainduced inflammatory response was reflected by a markedly increased rolling and adherence of leukocytes, primarily restricted to the endothelium of postcapillary venules; this was accompanied by increased microvascular permeability, indicative of a substantial loss of endothelial integrity. The microcirculation surrounding the core of the damaged tissue area resembled that of ischemia\u2010reperfusion injury in skeletal muscle, i.e., heterogeneous capillary perfusion, pronounced microvascular leakage and adherence of leukocytes. Enhanced vascular leakage and leukocyte adherence (24\u201072 hours after injury) coincided with the maximum intramuscular pressure (which was not indicative of compartment syndrome) and edema formation. These results demonstrate that initial changes, leading to ultimate tissue death, after closed soft\u2010tissue injury are caused on the microcirculatory level. This standardized model provides further insight into microvascular pathophysiology and cellular interactions following closed soft\u2010tissue injury. Thus, it is an adequate tool for testing novel therapeutic interventions.<\/jats:p>","DOI":"10.1002\/jor.1100170509","type":"journal-article","created":{"date-parts":[[2005,2,24]],"date-time":"2005-02-24T10:32:02Z","timestamp":1109241122000},"page":"678-685","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":99,"title":["<i>In vivo<\/i> analysis of microcirculation following closed soft\u2010tissue injury"],"prefix":"10.1002","volume":"17","author":[{"given":"Klaus\u2010D.","family":"Schaser","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Brigitte","family":"Vollmar","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Michael D.","family":"Menger","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Lioba","family":"Schewior","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Stefan N.","family":"Kroppenstedt","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Michael","family":"Raschke","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Andreas S.","family":"L\u00fcbbe","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Norbert P.","family":"Haas","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Thomas","family":"Mittlmeier","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"311","published-online":{"date-parts":[[2005,2,18]]},"reference":[{"key":"e_1_2_1_2_2","first-page":"122","article-title":"Pathophysiology and related studies of the no reflow phenomenon in skeletal muscle","volume":"314","author":"Allen DM","year":"1995","journal-title":"Clin Orthop"},{"key":"e_1_2_1_3_2","first-page":"437","article-title":"Cerebral ischemia. 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