Sympathetic control of pulmonary vascular impedance in anesthetized dogs.

The effects of left stellate ganglion stimulation on pulmonary hydraulic input impedance was evaluated in 21 experiments on open-chest dogs anesthetized with chloralose. The stellate ganglion was stimulated at 1, 2, 5, 10, and 20 cps, and impedance spectra were generated at each frequency. Control spectra were characterized by frequency-dependent oscillations in impedance magnitude. Generally, impedance minimums occurred between 2 and 3 cps and maximums between 4 and 6 cps. Stellate ganglion stimulation caused elevations in impedance magnitude and shifted the impedance curve upward. The average control impedance magnitude at the minimum was 4780 dyne sec cmkg ± 262 SE and was increased to 8280 ± 452 during stimulation at 20 cps, while the frequency of the first harmonic in the control averaged 2.50 ± 0.08 SE cps and was 3.10 ± 0.08 during stimulation at 20 cps. Maximum activation of sympathetic outflows (10—20 cps) caused the impedance curve to flatten, attenuating frequency dependent oscillations characteristic of control spectra. The administration of propranolol attenuated cardiogenic increases in pulmonary pressure and flow during stellate ganglion stimulation, but elevations in pulmonary vascular impedance still occurred, indicating that this was not dependent on changes in harmonic content of the flow pulse that attended changes in heart rate and stroke volume. Frequency dependent oscillations in impedance magnitude were usually enhanced during left stellate ganglion stimulation following propranolol. The results indicate that sympathetic nerve stimulation increases the opposition to pulsatile flow; since pulmonary vascular resistance was relatively less affected, the input impedance becomes a greater fraction of the total opposition that must be overcome in moving blood through the lungs.