EFFECTS OF STATIC LUNG-INFLATION ON SYMPATHETIC ACTIVITY IN HUMAN MUSCLE NERVES AT REST AND DURING ASPHYXIA

Muscle sympathetic activity is inhibited during the second half of pha sic lung inflation associated with normal (negative pressure) breathin g or artificial ventilation with intermittent positive-pressure, and t his inspiratory inhibition appears unrelated to the associated changes in arterial pressure. In the present study we tested the hypothesis t hat a static inflation of the lungs would cause a sustained inhibition of muscle sympathetic activity. Microneurographic techniques were use d to record muscle sympathetic activity from the peroneal nerve, and a rterial pressure was monitored continuously by finger-pulse photopleth ysmography (Finapres). In nine subjects static lung inflation, brought about either actively or passively, caused a pronounced and sustained increase in sympathetic activity (not the predicted decrease) that co uld not be explained by changes in arterial pressure. When delivered a t the end of a voluntary end-expiratory apnoea, static lung inflation caused an initial inhibition of the large chemoreceptor-induced sympat hetic bursts and a subsequent excitation that was sustained for the du ration of the lung inflation. These observations indicate that respira tion can affect muscle sympathetic activity in humans in two opposing ways: inhibition during phasic increases in lung volume, and excitatio n during large static increases in lung volume. Neither phenomenon dep ends on changes in arterial pressure, and hence influences of carotid arterial and aortic (high-pressure) baroreceptors can be excluded. We suggest that the initial inhibition is evoked from lung or chest-wall receptors and the static exitation from unloading of cardiopulmonary ( low pressure) baroreceptors.