Iloprost in Experimental Cerebral Ischemia

End-products of arachidonic acid cascade are known to play a role in platelet aggregation and may also be involved in the pathogenesis of various cerebral dis-eases related to ischemia. The transformation of arachidonic acid into thromboxane A2 (TXA2) occurs via the production of intermediate products called endoperoxides. Apart from the effects of TXA2, it is now well known that healthy vessel walls readily transform endoperoxides into an unstable substance which is a potent vasodilator and inhibitor of platelet aggregation. This compound, originally called PGX by Moncada et al. [17, 18], and Gryglewski et al. [12], has been renamed prostacyclin or PGI2 [16]. Its pharmacological properties led us to hypothesize that PGI2 and some stable prostacyclin analogues, such as Iloprost, may be helpful in improving the postischemic disease in which platelet aggregation and vascular spasms are particularly involved, as well as in reducing the seconday decrease in cerebral blood flow called “delayed hypoperfusion” which succeeds the initial reactive hyperemia [14]. The aim of this study has been to investigate on one hand the curative effect of Iloprost on the neurologic deficit, the electrolyte unbalance and the impairment of brain function which develop in the subacute period (3 days) following a transient cerebral oligemia in the rat [3, 4]; and on the other hand its effect upon the hemodynamic and metabolic consequences of a transient cerebral ischemia in the dog over the acute phase (2 h) following subtotal occlusion of carotid and vertebral arteries [7].