In seven anesthetized dogs that had been prepared with a bilateral cervical vagotomy, an RSA simulation model was created after the elimination of endogenous autonomic activities by means of a reserpine injection.7
Respiration-linked heartbeat fluctuations were generated by electrical stimulation of the right cervical vagi, whereas negative pressure ventilation was generated by the diaphragm pacing technique (so-called electrophrenic respiration) to mimic spontaneous breathing.,11
During inspiration, the phrenic nerve was electrically paced to generate negative intrathoracic pressure, to preserve the physiologic respiratory pump effects on venous return. During expiration, the pressure in the thorax was equal to the atmospheric pressure. Vagal stimulation was performed under the following three conditions: phasic stimulation during expiration (artificial RSA; Fig 3
, top); inspiration (inverse RSA; Fig 3
, bottom); and constant stimulation (control) causing the same number of heartbeats per minute as artificial and inverse RSA. We found that artificial RSA decreased both of the ratios of physiologic dead space to tidal volume and physiologic shunt to cardiac output by 10% and 51%, respectively, but increased O2 uptake by 4% compared with the control. In contrast, we also found that inverse RSA increased the ratios of both physiologic dead space to tidal volume and physiologic shunt to cardiac output by 14% and 64%, respectively, and decreased O2 uptake by 14% compared with the control. Under these three conditions, the tidal volume, minute ventilation, heart rate, cardiac output, and arterial BP were all unchanged. Our results may well support the hypothesis that RSA improves the pulmonary O2 uptake (ie, the pulmonary gas exchange) by matching perfusion to ventilation within each respiratory cycle, and, hence, suppressing unnecessary heartbeats during expiration and ineffective ventilation during the ebb of perfusion.