Vagal cardiopulmonary reflexes after total cardiac deafferentation

Background-There are conflicting data regarding whether the primary source of efferent input for the vagal cardiopulmonary reflex emanates from recept ors located in the ventricles, atria, and/or lungs. This study evaluated th e effects of total cardiac deafferentation on the reflex control of efferen t renal sympathetic nerve activity (RSNA) in response to a stimulus that af fected all vagal receptors in the cardiopulmonary region. Methods and Results-Experiments were performed in 14 chloralose-anesthetize d dogs with sinoaortic denervation. Reflex control of RSNA in response to b lood volume expansion was measured before and after interruption of cardiac vagal afferents by pericardial lidocaine (PL). Reflex sensitivity (% chang e in RSNA/mm Hg change in left atrial pressure) was markedly attenuated aft er PL (pre, -10.9+/-2.2; post, -1.6+/-0.6; P=0.002). RSNA responses to intr acoronary nicotine and left atrial balloon inflation were abolished after F L, confirming that cardiac afferents were interrupted, RSNA responses to lu ng inflation were not affected by FL, indicating that pulmonary afferents r emained intact. In 8 experiments, reflex sensitivity values returned to bas eline levels after the effects of PL had worn off. Conclusions-These results indicate that the heart provides the primary sour ce of afferent input for the control of sympathetic outflow by the vagal ca rdiopulmonary reflex during changes in thoracic blood volumes and pressures .