The Effect of Indomethacin on Ischemic Brain Edema : A Study Using Cat Middle Cerebral Artery Occlusion Combined with Recirculation

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The role of the arachidonate cascade in the development of ischemic edema was studied using indomethacin, an inhibitor of cyclooxygenase. Cortical specific gravity (SG) was measured in cats after middle cerebral artery (MCA) occlusion. The cats were divided into five groups: Groups 1 and 2-two and four hour MCA occlusion; Group 3-two hour MCA occlusion followed by two hour MCA recirculation; Group 4-two hour MCA occlusion followed by two hour MCA recirculation with preadministration of indomethacin (4 mg/kg, i.v.); and Group 5-four hour MCA occlusion with indomethacin. The local cerebral blood flow (1CBF) was measured periodically with cortical electrodes by the hydrogen clearance method. At the end of the experiment, the SG of the cerebral cortex surrounding each electrode was measured using a gradient column. Indomethacin caused a generalized 1CBF reduction of about 16%. During occlusion as well as recirculation, however, there was no significant difference in 1CBF between the indomethacin-treated and -untreated groups. A significant reduction in the SG was observed in all groups accompanying profound ischemia (1CBF less than 20 ml/100 g/min). Compared with continuous MCA occlusion (Groups 1 and 2), recirculation resulted in further reduction in the cortical SG (Group 3). This recirculation-induced reduction in the SG was almost completely prevented by the indomethacin pretreatment (Group 4). In Group 5, indomethacin further reduced the cortical SG. The above results indicate that the arachidonate cascade is involved in the aggravation of cerebral edema following the onset of recirculation.
日本脳神経外科学会の論文
1984-01-15

The Effect of Indomethacin on Ischemic Brain Edema : A Study Using Cat Middle Cerebral Artery Occlusion Combined with Recirculation

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