Palombo J D, Bowers J L, Clouse M E, McCullough A, Forse R A, Bistrian B R
Department of Surgery, New England Deaconess Hospital-Harvard Medical School, Boston, MA 02215.
Am J Clin Nutr. 1993 Mar;57(3):420-7. doi: 10.1093/ajcn/57.3.420.
The study objective was to assess hepatic utilization of exogenous adenosine or adenine to enhance ATP recovery in rat liver after cold ischemia. ATP was measured noninvasively by 31P nuclear magnetic resonance (NMR) in perfused livers before and after 18 h of cold ischemia. The hepatocellular concentration of ATP during the initial postischemic reperfusion without adenosine or adenine coinfusion was 60% of that in fresh liver. The ATP increased significantly (P < 0.001) to 139% and 82% of baseline in postischemic livers coinfused for 90 min with adenosine or adenine (final concentration, 1 mmol/L), respectively. Less than 0.5% of the excess adenosine was catabolized to uric acid. In conclusion, adenosine and, to a lesser extent, adenine are salvaged by liver after extended cold ischemia to enhance ATP restoration. Provision of these ATP precursors, as components of an enteral formulation may facilitate the repletion of liver ATP and foster early resumption of liver function after an ischemic insult.
本研究的目的是评估外源性腺苷或腺嘌呤在冷缺血后对大鼠肝脏的利用情况，以提高肝脏三磷酸腺苷（ATP）的恢复水平。在冷缺血18小时前后，通过31P核磁共振（NMR）对灌注肝脏中的ATP进行无创测量。在初始缺血后再灌注期间，未同时输注腺苷或腺嘌呤时，肝细胞内ATP浓度为新鲜肝脏的60%。在缺血后肝脏中，分别与腺苷或腺嘌呤（终浓度为1 mmol/L）同时输注90分钟后，ATP显著增加（P < 0.001），分别达到基线水平的139%和82%。不到0.5%的过量腺苷被分解代谢为尿酸。总之，在长时间冷缺血后，肝脏能利用腺苷，腺嘌呤的利用程度稍低，以提高ATP的恢复。作为肠内制剂的成分提供这些ATP前体，可能有助于补充肝脏ATP，并促进缺血损伤后肝功能的早期恢复。
