Effects of propranolol on the cardiovascular and renin-angiotensin systems during hypotension produced by sodium nitroprusside in humans.

The authors examined the effects of controlled hypotension induced with sodium nitroprusside (SNP) with and without propranolol on the cardiovascular, pulmonary, and renin-angiotensin systems in 10 consecutive anesthetized patients with kyphoscoliosis undergoing posterior spinal fusion. SNP infusion (4.1 microgram . kg-1 . min-1) alone decreased mean systemic arterial pressure (SAP) by 25 torr +/- 3 SE (P less than 0.001), systemic vascular resistance index (SVRI) by 1113 dyne . sec. cm-5 . m2 +/- 125 SE (P less than 0.001), mean pulmonary artery pressure (PAP) by 6 torr +/- 2 SE (P less than 0.02), pulmonary capillary wedge pressure (PCWP) by 4 torr +/- 1 SE (P less than 0.01), pulmonary vascular resistance (PVR) by 50 dyne . sec . cm-5 +/- 18 (P less than 0.05), and PaO2 by 16 torr +/- 7 SE (P less than 0.05), whereas cardiac index increased by 1.08 l . min-1 . m2 +/- 0.24 SE (P less than 0.01) and heart rate increased 16 beats/min +/- 5 SE (P less than 0.02). After 40 min of hypotension, 0.03 mg/kg propranolol was injected intravenously while the SNP infusion rate was held constant. Ten min later there was a significant decrease in the heart rate (10 beats/min +/- 4 SE, P less than 0.02) and cardiac index (0.65 l . min-1 . m-2 +/- 0.21, P less than 0.02). Plasma renin activity (PRA) increased from 2.37 ng . ml-1 . h-1 +/- 0.7 SE before anesthesia to 6.50 ng . ml-1 . h-1 +/- 1.45 SE (P less than 0.05) after 40 min of nitroprusside infusion. Forty min after propranolol there was a significant reduction in PRA to 4.07 ng . ml-1 . h-1 +/- 0.73 SE (P less than 0.05). Thus propranolol, when given during SNP hypotension, exhibits an early cardiovascular response manifested as a decrease in cardiac output and heart rate and a delayed action of the kidney resulting in an inhibition of renin release.