The purpose of this study was to demonstrate the effect of allopurinol on ischemia and reperfusion-induced cerebral injury and to investigate the importance of xanthine oxidase (XO)-linked free radical in cerebral injury. Acute focal cerebral ischemia was induced by occlusion of the left middle cerebral artery(MCA). The experimental animals were divided into three groups. The group I was the sham control and group II the cats of 4-hour occlusion and recirculation. The Group III, The treatment group, was given allopurinol (50mg/kg) of peritoneal injection 2 hours prior to the occlusion of the MCA. The brain tissue of left MCA territory was removed, and homogenate was made. Supernatent and cytoplasm were obtained by centrifuge 30min at 3,000rpm(4℃), and recentrifuge 20min at 11,000rpm(4℃), respectively XO activities were measured in all samples by spectrophotometer. The XO activities was increased in group II. allopurinol significantly suppressed the XO activities in group III. It suggested that the XO may play important role in the pathogenesis of isechemic injury of cat brain and allopurinol could be used as therapeutic agents in the clinical field of the focal cerebral ischemical patients.

The purpose of this experimental study is to determine the protective effect of pretreatment of mannitol, methylprednisolone, thiopental sodium and nimodipine against the acute focal cerebral ischemia. The energy metabolisms of the brain was measured utilizing the high liquid performance chromatography in the brain tissues of the cats. The experimental animals were separated into three groups. In group I (the sham control group) the middle cerebral artery(MCA) was not occluded. In group II (the recirculation group) the MCA was occluded for 5 hours and reperfused for 2 hours. In group III (the treatment group) the combinations of mannitol(2gm/kg), methylprednisolone(30mg/kg), and thiopental sodium(5mg/kg) were administered intravenously at 30 minutes before occlusion of the MCA. The mannitol and methylprednisolone were repeated every one and half hours and thiopental sodium every hours. Nimodipine(3µg/kg/min) was continuously intravenous infused during 7 hours, initiated 30minutes before induction of ischemia.

The experimental results are as follows.

1) Adenosine derivatives : In group III ATP and ADP were very highly signficantly increased to 485.35% and 218.45% respectively and the total adenylate to 170.27% of the value of group II. AMP reduced to 62.62% of the value of the group II.

2) Adenylate energy charge(E.C.) : In group III E.C. was increased to 196.67% of the value of group II and recoveried to 78.67% of the group I.

3) GTP and total guanylate : In group III GTP and total guanylate were very-highly signficantly increased to 351.55% and 241.22% of the value of the gorup II respectively.

4) UTP and total uridylate : In group III UTP and total uridylate were highly signficantly increased to 4296.30% and 222.22% of the value of the group II, respectively.

The above results suggest that the pretreatment of this therapeutic combination of the drugs may have an effective means of treating actue focal cerebral infarction and would be applicable in the clinical field in which the ischemia is anticipated during major cerebral artery occlusion.