Abstract：Objective Some research has shown that the inflammatory reaction induced by the intercellular adhesion molecule may be involed in ischemic renal injury. Intercellular adhesion molecule-1 (ICAM-1) plays an important role in renal injury by up-regulating and inducing the adhesion between white blood cells and endothelium. This paper aims to study the effect of ICAM-1 on the inflammatory reaction in the fetal rat kidneys after acute ischemia. Methods The models of intrauterine ischemia and reperfusion in various time points were established by clamping one side of the vessels supplying blood to uterus in 21-gestational day-old Wister rats. The dynamic changes of ICAM-1 in the fetal kidneys were detected by immunohistochemical technique. Meanwhile, renal histopathological changes were observed. Another group of rats, the Sham-operation group, were given a normal blood supplement in the other side of the uterus. Results There was a small quantity expression of ICAM-1 in the cortical tubuli, especially in the proximal tubuli, in the Sham-operation group. The ICAM-1 expression began to increase 35 and 45 minutes after ischemia (P< 0.05). Compared with that of the Sham-opereation group, after a 15-minute ischemia and then a 2-hr repefusion, it began to rise (P< 0.01), reached a peak at 15 hrs of reperfusion (P< 0.01) and remained a higher level till 30 hrs of reperfusion (P< 0.05). Histological changes were most prominent after a 15-minute ischemia and then a 15-hr reperfusion, including vascular congestion, tubular vacuolar degeneration or necrosis and neutrophil accumulation. Conclusions There may be an inflammatory reaction in renal injury induced by intrauterine ischemia and reperfusion. Ischemia and reperfusion can induce the elevation of ICAM-1 expression. This suggests that ICAM-1 may play an important role in the development of inflammatory reaction in renal injury induced by acute ischemia and hypoxia.
WU Jie,YANG Li,WEI Ke-Lun. Expression of intercelluar adhesion molecule-1 in the fetal kidneys of rats after intrauterine acute ischemia and hypoxia[J]. CJCP, 2004, 6(3): 199-202.
