Several of the cyclooxygenase products of arachidonic acid were measured in the cerebral hemispheres of gerbils subjected to transient interruption of the cerebral circulation. The levels of PGD2, PGF2 alpha, PGE2, TXB2, 13, 14-H2-15-keto-PGE2, and the stable nonenzymic product of prostacyclin, 6-keto-PGF1 alpha, were not altered at the end of a 5-min period of ischemia. However, the onset of reperfusion was accompanied by a rapid accumulation of these products. Levels were highest during the initial period of reperfusion, then decreased to approach control levels after 120 min. PGD2, PGF2 alpha, and PGE2 were the predominant metabolites detected. This postischemic accumulation of arachidonic acid metabolites could be blocked by prior administration of inhibitors of cyclooxygenase activity.

No abstract

Aktmct-Cortical monoamine changes during ischemic episodes of varied duration and their sequence of changes following cerebral reperfusion were studied in the gerbil. Forty-one percent of 280 animals exhibited signs of cerebral hemispheric ischemia (stroke) after unilateral common carotid artery occlusion. Norepinephrine (NE) levels decreased after 60 min in the occluded hemisphere of stroked animals but dopamine (DA) levels were unaltered. 5-Hydroxytryptamine (5-HT) levels became bilaterally reduced in both stroked and non-stroked animals as soon as 5 min after occlusion.Upon reperfusion after periods of 30 or 60 min of occlusion there was a bilateral rebound increase of cortical NE and DA levels to well above control values in stroked and non-stroked animals. 5-HT levels remained reduced in both groups.

The concentrations of the arachidonic acid metabolites, PGD2, PGF2 alpha and 6-keto-PGF1 alpha, were measured in the cerebral hemispheres of gerbils subjected to unilateral carotid occlusion. Approximately 37 percent of the animals with occlusion had symptoms of cerebral ischemia. In those animals PGD2 and PGF2 alpha levels were elevated in both hemispheres. The levels of 6-keto-PGF1 alpha increased only slightly. There was no change of prostaglandin levels in asymptomatic animals. Indomethacin inhibited the increase in the levels of these arachidonic acid metabolites but did not alter brain swelling as judged by a decrease in specific gravity after 6 hours occlusion.

SYNOPSISCentral pain supersensitivity related to depletion of serotonin in the central nervous system has been postulated as a mechanism for migraine. In the present study, transient cerebral ischemia in an animal preparation caused depletion of central nervous system serotonin. Ischemia associated with the prodromal phase of migraine must, therefore, be considered as a possible cause of altered central nervous system serotonin metabolism, possibly leading to increased pain sensitivity.