Discontinuous total parenteral nutrition prevents postischemic mitochondrial dysfunction in rat liver
Discontinuous total parenteral nutrition prevents postischemic mitochondrial dysfunction in rat liver
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不连续全肠外营养可预防大鼠肝脏缺血后线粒体功能障碍
DOI：
10.1002/hep.510280518
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发表时间：
1998
期刊：
影响因子：
13.5
通讯作者：
Masaki Kitajima
中科院分区：
文献类型：
--
作者：
N. Morikawa;M. Suematsu;T. Kyokane;N. Goda;Y. Kumamoto;Taro Okitsu;Y. Ishimura;Masaki Kitajima
尽管近年来间断全肠外营养(d-TPN)在改善肝功能方面优于连续全肠外营养(c-TPN)，但对术后肝功能障碍的保护机制尚不清楚。本研究旨在检测d-TPN和c-TPN处理的肝脏在缺血再灌流过程中线粒体功能的差异。经d-TPN或c-TPN处理的大鼠肝脏用Krebs-Ringer缓冲液灌流，暴露于25%低流量低氧中，然后再灌流。用罗丹明123(Rh123)和碘化丙啶(PI)双色数字荧光显微镜检测肝内线粒体膜电位(▵Ψ)和细胞存活率。作为对低氧的响应，c-TPN、d-TPN和普通饲料预处理的肝脏显示出整个小叶中▵Ψ的显著减少。再灌流后，c-TPN组大鼠肝脏局部▵Ψ值进一步降低，而d-TPN组或食物处理组大鼠肝脏局部TPN值迅速恢复至对照水平。细胞损伤的严重程度在不同组之间没有差异，表明c-TPN预处理的肝脏再灌流引起的▵Ψ下降不是细胞损伤的结果。不同组间▵Ψ下降的差异似乎与糖原储存的差异无关，因为接受d-TPN的肝脏即使在禁食状态结束时再灌流时也显示出显著的▵Ψ恢复。这些结果表明，c-TPN，而不是d-TPN，危及线粒体的重新充能，提示TPN的昼夜节律模式是降低肝脏缺血后线粒体功能障碍风险的潜在有益策略。
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.
用于评估灌注大鼠肝脏缺氧引起的区域特异性损伤的新的简单模型：时间进程和营养状态的影响。
DOI：
--
发表时间：
1986
期刊：
The Journal of pharmacology and experimental therapeutics
影响因子：
--
作者：
Bradford,BU;Marotto,M;Lemasters,JJ;Thurman,RG
通讯作者：
Thurman,RG
DOI：
10.1016/0005-2728(86)90112-x
发表时间：
1986-07-23
期刊：
BIOCHIMICA ET BIOPHYSICA ACTA
影响因子：
--
作者：
EMAUS, RK;GRUNWALD, R;LEMASTERS, JJ
通讯作者：
LEMASTERS, JJ
影响因子：
--
作者：
GORES, GJ;FLARSHEIM, CE;LEMASTERS, JJ
通讯作者：
LEMASTERS, JJ