Xanthine and Uric Acid Levels in Rat Brain Following Focal Ischemia

Abstract

Changes of the xanthine and uric acid (UA) levels in rat forebrain following focal cerebral ischemia were studied by reversed-phase HPLC with electrochemical detection. Focal ischemia was induced by occluding the left middle cerebral artery in the rat. The xanthine level in the normal group was 11.50 nmol/g tissue. In the ischemic group, the xanthine concentration in the ischemic hemisphere progressively increased after occlusion and reached a maximum value of 59.42 nmol/g tissue 4 h after operation. The UA level in the normal group was 2.20 nmol/g tissue, whereas in the ischemic group the UA concentration in the ischemic hemisphere gradually increased after occlusion, reaching a value of 38.53 nmol/g tissue 24 h after ischemia. The concentration of UA remained elevated in the ischemic hemisphere until 48 h after occlusion, and reached a maximum value of 38.98 nmol/g tissue. The xanthine and UA levels in the contralateral hemisphere remained unchanged. The xanthine and UA concentrations in the sham-operated group did not show a significant increase after operation. The time course of xanthine and UA levels suggests that in ischemic forebrain UA is formed from xanthine as a product of purine metabolism.

Extracellular Antioxidants and Amino Acids in the Cortex of the Rat: Monitoring by Microdialysis of Early Ischemic Changes

“…The striatal EC con centrations of precursors of VA (adenosine, inosine, and hypoxanthine) increased markedly on the occluded side following MCAO (Hillered et al, 1989). The levels of VA in tissue homogenates of the affected cerebral hemisphere were also reported to rise slowly and to be still rising 4 h after surgery (Kanemitsu et al, 1988). Although our results did not reach statistical significance, the slow and steady increase in V A following focal ischemia showed the expected trend.…”

Neurochemical analysis of focal ischemia in rats.

“…6 -7 However, we did not observe increased xanthine levels immediately after the ischemia, as was reported previously. 6 This difference may reflect the different models of ischemia in the two studies. The study of Kanemitsu et al 6 used permanent occlusion of the MCA by a transretroorbital approach, whereas in our study the MCA was ligated and ischemia induced by common carotid artery occlusion followed by reperfusion.…”

The urate and xanthine concentrations in the cerebrospinal fluid in patients with vascular dementia of the Binswanger type, Alzheimer type dementia, and Parkinson's disease

“…An increase in the urate concentration has been demonstrated in the CSF of patients with ischemic brain disease (Hfillgren et al, 1983), and also in experimental ischemia in rat (Kanemitsu et al, 1988), which was inhibited by allopurinol (Nihei et al, 1989). The observed increase in the urate concentration in VDBT patients may be largely related to a disturbance of the BBB, because the urate concentration in the CSF had a nonsignificant trend to have a positive correlation with that in serum, and because the UcsF/Userum ratio was increased independently of the UCSF/ XCSF ratio.…”