Cerebral vasospasm and free radicals.

The literature implicating free radical reactions in the genesis of cerebral vasospasm following aneurysmal subarachnoid hemorrhage is reviewed. While this condition has features of a prototypical free radical-mediated disease and a plausible theory can be outlined, data to support the theory are limited. An association of lipid peroxidation with vasospasm has been observed, but more sophisticated techniques for detection of free radicals and for detection of free radical damage to arterial wall proteins and nucleic acids have not been used. There are conflicting reports about efficacy of various antioxidant treatments for vasospasm. In these studies, concomitant experiments have usually not confirmed that the treatments have decreased free radicals or lipid peroxides in cerebrospinal fluid. Because smooth muscle contraction is involved in vasospasm, it would be interesting to investigate the actions of free radicals on smooth muscle cells using, for example, isometric tension recordings and patch clamp techniques. Studies of cardiac myocytes indicate that free radicals alter conductances through potassium and calcium channels and through the sodium-calcium exchanger and may result in elevations in intracellular calcium. Few studies have been performed on cerebral smooth muscle cells. In one study, exposure of cerebrovascular smooth muscle cells to free radicals resulted in increased outward currents, decreased membrane resistance, cell contraction, appearance of membrane blebs, and cell death. In summary, more investigations using better experimental techniques are required before free radicals and reactions induced by them can be said with certainty to be the primary cause of vasospasm.