Discontinuous Total Parenteral Nutrition Prevents Postischemic Mitochondrial Dysfunction in Rat Liver

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Abstract
Although discontinuous total parenteral nutrition (d–TPN) has recently been favored for clinical use over continuous total parenteral nutrition (c–TPN) 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–TPN– and c–TPN-pretreated livers during ischemia–reperfusion. Rat livers pretreated with d–TPN or c–TPN were perfused with Krebs–Ringer buffer and were exposed to 25% low–flow hypoxia followed by reperfusion. Intrahepatic mitochondrial membrane potential (△Ψ) and cell viability were assessed by dual–color digital microfluorography using rhodamine 123 (Rh123) and propidium iodide (PI), respectively. In response to hypoxia, livers pretreated with c–TPN, d–TPN, and an ordinary chow diet exhibited a significant △Ψ reduction among the entire lobules. Upon reperfusion, the regional △Ψ values further decreased in the c–TPN liver, whereas those in the d–TPN-treated or chow–treated livers displayed a rapid recovery toward the control levels. The severity of cell injury did not differ among the groups, showing that the reperfusion–induced △Ψ drop in the c–TPN-pretreated liver is not a consequence of cell injury. Differences in the △Ψ drop among the groups appear to occur irrespective of those in the glycogen storage, because the livers undergoing d–TPN display a marked △Ψ recovery even when reperfused at the end of a fasted state. These results indicate that c–TPN, but not d–TPN, jeopardizes mitochondrial re–energization 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.