{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,10,20]],"date-time":"2025-10-20T17:01:19Z","timestamp":1760979679930,"version":"3.30.0"},"reference-count":40,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"5","license":[{"start":{"date-parts":[[2015,9,1]],"date-time":"2015-09-01T00:00:00Z","timestamp":1441065600000},"content-version":"tdm","delay-in-days":6148,"URL":"http:\/\/doi.wiley.com\/10.1002\/tdm_license_1.1"}],"content-domain":{"domain":["lww.com","ovid.com"],"crossmark-restriction":true},"short-container-title":[],"published-print":{"date-parts":[[1998,11]]},"abstract":"<jats:sec>\n            <jats:title\/>\n            <jats:p>Although discontinuous total parenteral nutrition (d\u2013TPN) has recently been favored for clinical use over continuous total parenteral nutrition (c\u2013TPN) to ameliorate liver dysfunction, mechanisms for the protection against postoperative liver dysfunction remain unknown. This study aimed to examine differences in mitochondrial function in d\u2013TPN\u2013 and c\u2013TPN-pretreated livers during ischemia\u2013reperfusion. Rat livers pretreated with d\u2013TPN or c\u2013TPN were perfused with Krebs\u2013Ringer buffer and were exposed to 25% low\u2013flow hypoxia followed by reperfusion. Intrahepatic mitochondrial membrane potential (\u25b3\u03a8) and cell viability were assessed by dual\u2013color digital microfluorography using rhodamine 123 (Rh123) and propidium iodide (PI), respectively. In response to hypoxia, livers pretreated with c\u2013TPN, d\u2013TPN, and an ordinary chow diet exhibited a significant \u25b3\u03a8 reduction among the entire lobules. Upon reperfusion, the regional \u25b3\u03a8 values further decreased in the c\u2013TPN liver, whereas those in the d\u2013TPN-treated or chow\u2013treated livers displayed a rapid recovery toward the control levels. The severity of cell injury did not differ among the groups, showing that the reperfusion\u2013induced \u25b3\u03a8 drop in the c\u2013TPN-pretreated liver is not a consequence of cell injury. Differences in the \u25b3\u03a8 drop among the groups appear to occur irrespective of those in the glycogen storage, because the livers undergoing d\u2013TPN display a marked \u25b3\u03a8 recovery even when reperfused at the end of a fasted state. These results indicate that c\u2013TPN, but not d\u2013TPN, jeopardizes mitochondrial re\u2013energization and suggest that a circadian pattern of the TPN serves as a potentially beneficial strategy to reduce the risk of postischemic mitochondrial dysfunction in the liver.<\/jats:p>\n          <\/jats:sec>","DOI":"10.1002\/hep.510280518","type":"journal-article","created":{"date-parts":[[2004,7,27]],"date-time":"2004-07-27T23:30:02Z","timestamp":1090971002000},"page":"1289-1299","update-policy":"http:\/\/dx.doi.org\/10.1097\/lww.0000000000001000","source":"Crossref","is-referenced-by-count":12,"title":["Discontinuous Total Parenteral Nutrition Prevents Postischemic Mitochondrial Dysfunction in Rat 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