The systemic hemodynamic effects of deep hypotension (MAP: 38 +/- 6 mm Hg) induced by sodium nitroprusside (S.N.) were studied in 20 patients who underwent surgery for cerebral aneurysm. The hemodynamic measurements were performed four times.: (1) during the preoperative period, (2) during stable anesthesia just before hypotension, (3) during stable hypotension, (4) 20 minutes after stopping nitroprusside. All patients were mechanically ventilated with a constant tidal volume and rate. Parameters for acid-base balance and Pa O2 were also recorded. Nitroprusside produces arterial and venous dilatation which results in a decrease of afterload and preload. The mean dosage of S. N. was 18 mcg/kg/mn. Systemic vascular resistances decreased by 62 p. cent. Mean arterial pressure decreased by 53 p. cent; it reached 40 mm Hg. Fall in preload resulted in a decrease in pulmonary wedge pressure by 28 p. cent. This fall in preload produced a decrease in stroke index according to Frank-Starling's mechanisms. However tachycardia allowed a rise in cardiac index by 20 p. cent. Increase of pulmonary wedge pressure at 8-10 mm Hg by blood volume expansion maintains stroke index at control level. Under these conditions the elevation of cardiac index is due to tachycardia. Cardiac rhythm disorders (wandering pace-maker, nodal rhythm) are observed in 5 patients after having stopped nitroprusside.