Pathophysiology and basis of treatment of vasospasm.

The exact mechanism of vasospasm is still unknown. The etiology of cerebral vasospasm is subarachnoid blood clot. Vasospasm is a multifactorial proces s. Oxyhemoglobin is released by erythrocyte lysis and exert several effects on the endothelium that could lean to vasoconstriction. The production of free radical and superoxide anion radical secondary to he moglobin degradation stimulates the release of vasoconstricting products. A rterial vasoconstriction secondary to smooth muscle contraction could be re lated to increase in protein kinase C. Narrowing of cerebral vessels produc es cerebral ischemia by hemodynamic mechanisms. Direct hypothalamic insults may be associated. Clot removal and clot lysis have been proposed to prevent vasospasm. Pharma cological treatments are targeted to the vasospasm itself (nicardipine, AT8 77) or the prevention of delayed ischemic events (nimodipine, tirilazad). G eneral measures such as the <<triple H therapy>> (hemodilution, hypertensio n, hypervolemia) are widely used in the prevention and/or treatment of cere bral vasospasm.