{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,10,22]],"date-time":"2025-10-22T17:41:39Z","timestamp":1761154899580,"version":"3.32.0"},"reference-count":58,"publisher":"Wiley","issue":"2","license":[{"start":{"date-parts":[[2010,1,26]],"date-time":"2010-01-26T00:00:00Z","timestamp":1264464000000},"content-version":"vor","delay-in-days":1427,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Microcirculation"],"published-print":{"date-parts":[[2006,3]]},"abstract":"<jats:title>ABSTRACT<\/jats:title><jats:p><jats:bold>Objective:<\/jats:bold>Ischemic tolerance (IT) is known to improve resistance to ischemia\/reperfusion (I\/R)\u2010induced injury; however, the mechanisms remain unknown. The authors hypothesized that induction of heme oxygenase (HO), a heat shock protein, would provide anti\u2010inflammatory benefits during IT, thereby preventing leukocyte\u2010derived I\/R injury.<\/jats:p><jats:p><jats:bold>Methods:<\/jats:bold>Male Wistar rats were randomly assigned to sham (<jats:italic>n<\/jats:italic>= 4), I\/R (<jats:italic>n<\/jats:italic>= 9), preconditioning (PC)+I\/R (<jats:italic>n<\/jats:italic>= 7), chromium mesoporphyrrin, to inhibit HO (CrMP;<jats:italic>n<\/jats:italic>= 4), or PC+I\/R+CrMP (<jats:italic>n<\/jats:italic>= 6) groups. PC consisted of 5 cycles of I\/R, each lasting 10 min, induced by tightening a tourniquet placed above the greater trochantor of the hindlimb. Twenty\u2010four hours later, the hindlimb underwent 2 h of no\u2010flow ischemia followed by intravital microscopy during 90 min reperfusion to assess capillary perfusion (#\/mm), tissue injury (ratio of ethidium bromide to bisbenzimide labeled cells\/100 \u03bc m<jats:sup>2<\/jats:sup>), leukocyte rolling (Lr, #\/1000 \u03bc m<jats:sup>2<\/jats:sup>), and adhesion (La, #\/1000 \u03bc m<jats:sup>2<\/jats:sup>) in postcapillary venules of the extensor digitorum longus (EDL) muscle.<jats:bold>Results:<\/jats:bold>In the I\/R group, Lr was significantly increased (7.1 \u00b1 0.4) compared to sham (3.1 \u00b1 0.4). PC+I\/R increased Lr (10.8 \u00b1 0.72), which was further exacerbated by the removal of HO (14.2 \u00b1 1.3). La (7.8 \u00b1 2.0) was significantly increased compared to sham (2.4 \u00b1 0.9), while PC returned La back to sham levels (1.9 \u00b1 0.7). Removal of HO activity, via CrMP, had no significant effect on La (3.9 \u00b1 0.7). However, CrMP removed the protection to microvascular perfusion (I\/R = 9.4 \u00b1 1.1, PC = 16.6 \u00b1 1.8, sham = 20.5 \u00b1 2.8, PC+CrMP+I\/R = 12.3 \u00b1 2.3) and prevented protection from ischemia\u2010induced tissue injury.<\/jats:p><jats:p><jats:bold>Conclusion:<\/jats:bold>The data suggest that HO is an important protective mechanism during IT in skeletal muscle, but such protection was by mechanisms other than altered leukocyte\u2013endothelial cell interaction.<\/jats:p>","DOI":"10.1080\/10739680500466228","type":"journal-article","created":{"date-parts":[[2006,2,2]],"date-time":"2006-02-02T21:48:04Z","timestamp":1138916884000},"page":"71-79","source":"Crossref","is-referenced-by-count":8,"title":["Role of Heme Oxygenase in the Protection Afforded Skeletal Muscle During Ischemic Tolerance"],"prefix":"10.1111","volume":"13","author":[{"given":"ALISON 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