EXVIVO RELEASE OF EICOSANOIDS AFTER ANEURYSMAL SUBARACHNOID HEMORRHAGE - A PRELIMINARY EXPERIENCE IN HUMANS

Authors addressed the question whether the byosynthesis and the release of specific eicosanoids may occur in human brain cortex, and if the qualitative pattern of arachidonic acid metabolism is similar to that observed in experimental SAH. Human brain samples from 18 patients operated on for anterior communicating artery aneurysm (5 unruptured aneurysms considered as control cases, 7 patients operated on between Days 1 and 4 after SAH and 6 patients operated on between Days 10 and 14) were studied for the ex vivo release of 4 selected eicosanoids (Prostaglandin D2, E2, 6-keto-PGF1a and Leukotriene C4). Levels of arachidonate metabolites were determined by radioimmunoassay technique. PGD2 release is significantly lower in cases operated on delayed phase if compared to both control cases (p < 0.05) and patients operated on in the acute phase, while there is no significant difference between the release of PGD2 in control cases and patients operated on in the acute phase. Release of 6-keto-PGF1a is significantly higher in patients operated on in a delayed phase (p < 0.03 vs patients operated on in the acute phase and p < 0.05 versus control cases). The release of LTC4 is significantly enhanced (p < 0.05) in cases operated on in the acute phase if compared with unruptured aneurysms. The release of PGE2 is significantly enhanced in patients operated on in the acute phase (p < 0.05) if compared to patients with unruptured aneurysm. These results firstly confirm that in human brain tissue arachidonate metabolism is significantly enhanced after SAH, and suggest that the enhanced AA metabolism would be considered as an indirect ex vivo demonstration of the increased peroxidative processes caused by SAH.