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 cm-8 kg ± 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.
KEY WORDS propranololFourier analysis right ventricular function stellate ganglion stimulation pulmonary arteries• The pioneer studies of I. deB. Daly et al. demonstrated that sympathetic nerve stimulation increased the opposition to steady flow through artificially perfused lungs, thus establishing the existence of a sympathetic innervation to pulmonary vessels which could produce a direct vasomotor response (1 with stellate ganglion stimulation in isolated lung lobes perfused with pulsatile flow was an increase in arterial pulse pressure with an insignificant effect on the level of mean pressure (2). This resulted from generalized stiffening of large pulmonary arteries rather than from constriction of smaller muscular arterioles. Further studies showed that stellate ganglion stimulation reduced the volume distensibility of the main pulmonary artery and increased the elastic modulus of the arterial wall; thus these studies established a physical basis for the observed increases in pulsatile pressure (3).Since stiffening of conduit vessels tends to augment pressure pulsations, a major hemodynamic consequence of activation of sympathetic pathways to the pulmonary vasculature