OBJECTIVE: The purpose of this study was to investigate whether ischemia and subsequent reperfusion would affect xanthine oxidase activity in fetal rat brain capillaries. STUDY DESIGN: We used rats on day 19 of pregnancy. Fetal ischemia was induced by bilateral occlusion of the utero-ovarian artery for 20 minutes. Reperfusion was achieved by releasing the occlusion to restore the circulation for 30 minutes. Control rats underwent a sham operation. Fetal brain capillaries were isolated for measurement of concentrations of hypoxanthine, xanthine, and uric acid, as well as of concentrations of thiobarbituric acid-reactive substances. The brain capillaries were incubated with hypoxanthine for 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 hypoxanthine but had no effect on levels of xanthine, uric acid, and thiobarbituric acid-reactive substances. However, subsequent reperfusion led to significant increases in the levels of xanthine, uric acid, and thiobarbituric acid-reactive substances. Xanthine oxidase activity, as measured by the amount of xanthine produced, was significantly greater in the animals subjected to both ischemia and ischemia-reperfusion compared with the control group. CONCLUSION: Ischemic insult led to the accumulation of hypoxanthine and stimulated xanthine oxidase activity in fetal brain capillaries. Subsequent reperfusion enhanced the degradation of hypoxanthine to uric acid, which may induce cerebral lipid peroxidation.
OBJECTIVE: The purpose of this study was to investigate whether ischemia and subsequent reperfusion would affect xanthine oxidase activity in fetal rat brain capillaries. STUDY DESIGN: We used rats on day 19 of pregnancy. Fetal ischemia was induced by bilateral occlusion of the utero-ovarian artery for 20 minutes. Reperfusion was achieved by releasing the occlusion to restore the circulation for 30 minutes. Control rats underwent a sham operation. Fetal brain capillaries were isolated for measurement of concentrations of hypoxanthine, xanthine, and uric acid, as well as of concentrations of thiobarbituric acid-reactive substances. The brain capillaries were incubated with hypoxanthine for 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 hypoxanthine but had no effect on levels of xanthine, uric acid, and thiobarbituric acid-reactive substances. However, subsequent reperfusion led to significant increases in the levels of xanthine, uric acid, and thiobarbituric acid-reactive substances. Xanthine oxidase activity, as measured by the amount of xanthine produced, was significantly greater in the animals subjected to both ischemia and ischemia-reperfusion compared with the control group. CONCLUSION: Ischemic insult led to the accumulation of hypoxanthine and stimulated xanthine oxidase activity in fetal brain capillaries. Subsequent reperfusion enhanced the degradation of hypoxanthine to uric acid, which may induce cerebral lipid peroxidation.