[Pathophysiology and principles 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 process. Oxyhemoglobin is released by erythrocyte lysis and exert several effects on the endothelium that could lead to vasoconstriction. The production of free radical and superoxide anion radical secondary to hemoglobin degradation stimulates the release of vasoconstricting products. Arterial vasoconstriction secondary to smooth muscle contraction could be related to increase in protein kinase C. Narrowing of cerebral vessels produces cerebral ischemia by hemodynamic mechanisms. Direct hypothalamic insults may be associated. Clot removal and clot lysis have been proposed to prevent vasospasm. Pharmacological treatments are targeted to the vasospasm itself (nicardipine, AT 877) or the prevention of delayed ischemic events (nimodipine, tirilazad). General measures such as the "triple H therapy" (hemodilution, hypertension, hypervolemia) are widely used in the prevention and/or treatment of cerebral vasospasm.