Effect of sympathetic nerve stimulation on pulmonary vascular resistance in the dog.

The effect of sympathetic nerve stimulation on the pulmonary circulation was studied in a hemodynamically separated dog lung in which blood flow was maintained constant with a pump. Electrical stimulation of the stellate ganglia at 3, 10, and 30 cps produced a significant increase in mean lobar arterial perfusion pressure. Since lobar blood flow and left atrial pressure did not change during nerve excitation, the increase in lobar arterial pressure reflected an increase in vascular resistance across the lung. The increase in pulmonary vascular resistance was dependent on the stimulus frequency, and the time from the onset of stimulation to the attainment of the peak response was inversely related to the stimulus frequency. The response to nerve stimulation was decreased by alpha-receptor blocking agents. Lobar perfusion with a roller pump had an effect similar to perfusion with a piston pump. The response to nerve stimulation was independent of changes in rate, rhythm, and volume of respiration, changes in aortic blood pressure, and changes in airway resistance. The effects of stellate stimulation and of injected norepinephrine on vascular resistance were similar in the hemodynamically separated lobe. In essence, sympathetic nerve stimulation produced an active increase in vascular resistance in the pulmonary circulation, and the contribution of passive factors such as changes in respiration, bronchomotor tone, and bronchial circulation was minimal. Since the response was blocked by phentolamine, the increase in pulmonary vascular resistance in response to nerve stimulation was attributed to activation of alpha receptors in the pulmonary vascular bed by neurally released norepinephrine. These results demonstrate that pulmonary vascular resistance can be increased at stimulus frequencies in the physiological range of discharge for the sympathetic nervous system.