Effect of ischemia-reperfusion on xanthine oxidase activity in fetal rat brain capillaries

OBJECTIVE: The purpose of this study was to investigate whether ischemia an d subsequent reperfusion would affect xanthine oxidase activity in fetal ra t brain capillaries. STUDY DESIGN: We used rats on day 19 of pregnancy. Fetal ischemia was induc ed by bilateral occlusion of the utero-ovarian artery for 20 minutes. Reper fusion was achieved by releasing the occlusion to restore the circulation f or 30 minutes. Control rats underwent a sham operation. Fetal brain capilla ries were isolated for measurement of concentrations of hypoxanthine, xanth ine, and uric acid, as well as of concentrations of thiobarbituric acid-rea ctive substances. The brain capillaries were incubated with hypoxanthine fo r 1-5 hours at 25 degrees C. The activity of xanthine oxidase was estimated by measuring the amount of xanthine converted from hypoxanthine. RESULTS: Occlusion for 20 minutes markedly increased the concentration of h ypoxanthine but had no effect on levels, of xanthine, uric acid, and thioba rbituric acid-reactive substances. However, subsequent reperfusion led to s ignificant increases in the levels of xanthine, uric acid, and thiobarbitur ic acid-reactive substances. Xanthine oxidase activity, as measured by the amount of xanthine produced, was significantly greater in the animals subje cted to both ischemia and ischemia-reperfusion compared with the control gr oup. CONCLUSION: Ischemic insult led to the accumulation of hypoxanthine and sti mulated xanthine oxidase activity in fetal brain capillaries. Subsequent re perfusion enhanced the degradation of hypoxanthine to uric acid, which may induce cerebral lipid peroxidation.