{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,29]],"date-time":"2026-09-29T15:30:05Z","timestamp":1790695805655,"version":"4.1.0"},"reference-count":45,"publisher":"American Physiological Society","issue":"3","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Heart and Circulatory Physiology"],"published-print":{"date-parts":[[2003,9]]},"abstract":"<jats:p> Increased formation of reactive oxygen species (ROS) on reperfusion after ischemia underlies ischemia-reperfusion (I\/R) damage. We measured, in real time, oxygen tension in both microvessels and tissue and oxidant stress during postischemic reperfusion in the hamster cheek pouch microcirculation. We measured Po<jats:sub>2<\/jats:sub> by using phosphorescence quenching microscopy and ROS production in the systemic blood. We evaluated the effects of a nitric oxide synthase inhibitor ( N<jats:sup>G<\/jats:sup>-monomethyl-l-arginine, l-NMMA) and SOD on the oxidative stress during reperfusion. Microvascular injury was assessed by measuring diameter change, the perfused capillary length (PCL), and leukocyte adhesion. During early reperfusion, arteriolar Po<jats:sub>2<\/jats:sub> was significantly lower than baseline, whereas capillary Po<jats:sub>2<\/jats:sub> varied between 7 and 0 mmHg. Arterial blood flow did not regain baseline values, whereas Po<jats:sub>2<\/jats:sub> returned to baseline in arterioles and tissue after 30 min of reperfusion. During 5 and 15 min of reperfusion, ROS increased by 72 and 89% versus baseline, respectively, and declined to baseline after 30 min of reperfusion. Pretreatment with SOD maintained ROS at normal levels, increased arteriolar diameter, blood flow, and PCL, and decreased leukocyte adhesion ( P &lt; 0.05). l-NMMA decreased ROS only within 5 min of reperfusion, which increased significantly by 72% later during reperfusion. l-NMMA worsened leukocyte adhesion ( P &lt; 0.05). In conclusion, our results show that the early reperfusion is characterized by low Po<jats:sub>2<\/jats:sub> linked to increased production of ROS. At early reperfusion both SOD and l-NMMA decreased ROS production, whereas only SOD reduced it during later reperfusion. We suggest that low-flow hypoxia profoundly affects vascular endothelial damage during reperfusion through changes in ROS and nitric oxide production. <\/jats:p>","DOI":"10.1152\/ajpheart.00124.2003","type":"journal-article","created":{"date-parts":[[2015,3,3]],"date-time":"2015-03-03T20:11:53Z","timestamp":1425413513000},"page":"H1064-H1071","source":"Crossref","is-referenced-by-count":52,"title":["Microvascular oxygenation, oxidative stress, NO suppression and  superoxide dismutase during postischemic reperfusion"],"prefix":"10.1152","volume":"285","author":[{"given":"S.","family":"Bertuglia","sequence":"first","affiliation":[{"name":"Consiglio Nazionale delle Ricerca Institute of Clinical Physiology,  Medical School, University of Pisa, 56100 Pisa, Italy"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"A.","family":"Giusti","sequence":"additional","affiliation":[{"name":"Consiglio Nazionale delle Ricerca Institute of Clinical Physiology,  Medical School, University of Pisa, 56100 Pisa, Italy"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"24","reference":[{"key":"REF1","doi-asserted-by":"publisher","DOI":"10.1152\/ajpheart.01067.2001"},{"key":"REF2","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.87.4.1620"},{"key":"REF3","doi-asserted-by":"publisher","DOI":"10.1152\/ajpheart.2000.278.3.H755"},{"key":"REF4","doi-asserted-by":"publisher","DOI":"10.1006\/mvre.1995.1050"},{"key":"REF5","doi-asserted-by":"publisher","DOI":"10.1006\/mvre.2002.2400"},{"key":"REF6","doi-asserted-by":"publisher","DOI":"10.1007\/s001250100025"},{"key":"REF7","unstructured":"Bertuglia S,  Giusti A, and Pittman RN. 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