Prostacyclin attenuates in the rabbit hippocampus early consequences of transient complete cerebral ischemia

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Abstract
The effects of prostacyclin (PGI2) on ischemic changes of extracellular calcium concentration (CaE+2) and the blood-brain barrier (BBB) permeability were studied by microdialysis of the rabbit hippocampus. This was combined with morphological and neurophysiological observations. Complete cerebral ischemia lasting 15 min was produced by ligation of the brachiocephalic trunk, the left subclavian and both internal thoracic arteries. PGI2 was infused continuously i.v. in the last 3 min of ischemia and for 40 min after it, at a rate of 2 micrograms/kg/min. Control rabbits were submitted to untreated 15-min complete cerebral ischemia. The animals treated with PGI2 were found to have recovered bioelectric activity of the cortex and hippocampus in half the time that it took the untreated group. Application of PGI2 reduced by 60% the depth of ischemia-evoked drop of CaE+2 without acceleration of recovery during recirculation. The postischemic increase of BBB permeability to fluorescein was diminished. The number of morphologically changed neurons in the hippocampus of PGI2-treated animals was significantly lower than in the untreated group.