[The mechanisms of the ethomersol correction of postischemic hypoperfusion]. / Mekhanizmy korrektsii étomerzolom postishemicheskoi gipoperfuzii.

In rat experiments during brain ischemia (30-min carotid artery occlusion), ethomersol administered intraperitoneally in a dose of 50 mg/kg before occlusion or at the end of ischemia eliminated postischemic hypoperfusion. The effect of the drug was due to its spasmolytic and antiaggregatory activities. An analysis of the vasodilating action of ethomersol revealed its capacity to block potential-dependent calcium channels and partially intracellular calcium mobilization when the adrenergic and serotoninergic receptors were activated. The antiaggregatory activity of the drug appeared as inhibited platelet aggregation, which was induced by ADP, serotonin, arachidonic acid, thrombin, and as enhanced antiaggregatory activity of the vascular wall.

[Effects of ethomersol on cerebrovascular blood circulation and oxygen metabolism of the brain in acute transient ischemia and recirculation]. / Vliianie étomerzola na krovosnabzhenie i kislorodnyi obmen mozga pri ostroi tranzitornoi ishemii i retsirkuliatsii.

Intravenous infusion of ethomersol (50 mg/kg during 60 min) decreased cerebral tissue hypoxia at the end of acute cerebral ischemia in cats (30-min occlusion of both carotid and both vertebral arteries). In recirculatory period ethomersol prevented the postischemic hypoperfusion and especially hypo-oxygenation. Ethomersol-induced reduction of Hb-affinity to O2 was demonstrated.