[The role of nitric oxide and NO-synthase in the pathogenesis of cerebral damage after subarachnoid hemorrhage; laboratory models of subarachnoid hemorrhage].

Subarachnoid hemorrhage (SAH) of CNS is acute life-threating condition. In addition to its well understood sequential increase in intracranial pressure and decreased cerebral perfusion pressure, there is also early and late vasoconstriction. Mechanism of vasoconstriction is complex and one of important roles play changes in the amount of nitric oxide (NO). Present work overviews known pathogenesis of non-traumatic SAH, with stress on NO regulation of cerebral blood flow and its changes during SAH. It also describes mechanisms of early and late brain damage following subarachnoid hemorrhage. We discuss possible pharmacological prevention of the damage and laboratory models of nontraumatic SAH.