EXPERIMENTAL SUBARACHNOID HEMORRHAGE - EVENTS RELATED TO ANTIOXIDANT ENZYMATIC SYSTEMS AND EICOSANOID PEROXIDE ENHANCEMENT

Experimental and clinical studies have emphasized the role of free rad icals in the pathogenesis of vasospasm and neurological dysfunction af ter subarachnoid hemorrhage (SAH). Increases in both enzymatic (arachi donic acid cascade and eicosanoid peroxide production) and non-enzymat ic (tio-barbituric acid reactive substances production) lipid peroxida tion were found, pointing out the key role of arachidonic acid cascade in impairing membrane functionality in the post-hemorrhage brain. The aim of this work is to investigate whether a correlation exists betwe en time-dependent modifications of eicosanoid peroxide production (''e x vivo'' release of leukotriene C4 = LTC4) and antioxidant enzymatic s ystems in the brain after experimental subarachnoid hemorrhage in the rat. The release of the LTC4 is significantly enhanced at 1, 6 and 48 hours after SAH induction. Cu-Zn superoxide dismutase (SOD) activity i s significantly reduced at 6 and 48 hours after SAH induction; Mn-SOD activity is significantly affected at 1, 6 and 48 hours after the hemo rrhage. GSH-Px activity is significantly reduced only in the late phas e (48 hours) after SAH. The linear regression of statistical analysis, performed to investigate any possible relationship among time-depende nt modifications shows that the ''ex vivo'' release of LTC4 is signifi cantly related to the decreasing trend of MnSOD activity (p < 0.001). The present results suggest that after SAH, a deficit in endogenous an ti-oxidant defenses may play a role in making the brain more susceptib le to lipid peroxidative events.