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Ten patients who received hypotensive anesthesia for surgical correction of a cerebral aneurysm were pretreated for 1 day with propranolol. In the awake state, before start of anesthesia, mean arterial pressure was 91 ± 3 torr and plasma renin activity 3.0 ± 0.1 ng/ml/hr. Thirty minutes after the induction of anesthesia mean arterial pressure decreased to 79 ± 2 torr and plasma renin activity increased to 3.5 ± 0.1 ng/ml/hr. There was no further significant change in either measurement with surgical stimulation. During sodium nitroprusside-induced hypotension (the dose used was 0.35 ± 0.02 mg/kg) mean arterial pressure was reduced to 53 ± 2 torr, and plasma renin activity increased to 8.8 ± 0.9 ng/ml/hr. Heart rate did not change. Discontinuation of sodium nitroprusside resulted in a gradual reduction of plasma renin activity to the awake level and a concurrent gradual increase in mean arterial pressure to its basal anesthetic value. When compared with previous work, these results indicate that propranolol attenuates nitroprusside-induced renin release, reduces the dosage of nitroprusside required to induce hypotension, suppresses reflex tachycardia, and prevents overshoot hypertension on discontinuation of nitroprusside.