Karwinski W, Farstad M, Ulvik R, Sreide O
Surgical Research Laboratory, Haukeland Hospital, University of Bergen, Norway.
Eur Surg Res. 1992;24(5):257-64. doi: 10.1159/000129214.
A rat liver normothermic ischemia-reperfusion model was used to investigate whether hypoxanthine (HXA) that accumulated during ischemia was washed out in hepatic veins during reperfusion. Ischemia was induced in median and left lobes by clamping of the proper hepatic artery and portal branches. The effect of allopurinol (ALL) on metabolism of ATP and HXA was studied before, during and after a 60-min normothermic ischemic insult. Liver cell concentration of HXA in the group treated with ALL increased during ischemia and decreased rapidly during the first 10-min reperfusion. Recovery of ATP increased gradually during the 10-min reperfusion period and was significantly higher in the group treated by ALL compared to that of controls. Liver venous blood concentration of HXA in the ALL-treated group was 10-to 40-fold lower than that in liver tissue. The rapidly decreasing concentration of HXA in liver tissue during reperfusion and a minimal washout may indicate that HXA was used for resynthesis of ATP during reperfusion.
采用大鼠肝脏常温缺血再灌注模型，研究缺血期间积累的次黄嘌呤（HXA）在再灌注期间是否在肝静脉中被清除。通过夹闭肝固有动脉和门静脉分支诱导中叶和左叶缺血。在60分钟常温缺血损伤前、期间和之后，研究了别嘌呤醇（ALL）对ATP和HXA代谢的影响。ALL治疗组的肝细胞HXA浓度在缺血期间增加，在再灌注的前10分钟迅速降低。ATP的恢复在10分钟再灌注期逐渐增加，ALL治疗组明显高于对照组。ALL治疗组的肝静脉血HXA浓度比肝组织低10至40倍。再灌注期间肝组织中HXA浓度迅速降低且清除极少，这可能表明HXA在再灌注期间用于ATP的重新合成。
