Key result
Interruption of cardiac vagal afferents by pericardial lidocaine markedly attenuated reflex sensitivity of renal sympathetic nerve activity (-1.6 vs -10.9 pre-intervention; P=0.002).
Why the study?
Does total cardiac deafferentation by pericardial lidocaine affect the reflex control of efferent renal sympathetic nerve activity in response to blood volume expansion in anesthetized dogs?
Does total cardiac deafferentation by pericardial lidocaine affect the reflex control of efferent renal sympathetic nerve activity in response to blood volume expansion in anesthetized dogs?
Absolute Event Rate: -1.6% vs -10.9%
p-value: p=0.002
The heart provides the primary source of afferent input for the control of sympathetic outflow by the vagal cardiopulmonary reflex during changes in thoracic blood volumes and pressures.
Cardiac vagal afferents mediate volume-induced renal sympathetic inhibition in dogs; leaves open translation to human heart failure or volume overload.
BACKGROUND: There are conflicting data regarding whether the primary source of afferent input for the vagal cardiopulmonary reflex emanates from receptors located in the ventricles, atria, and/or lungs. This study evaluated the effects of total cardiac deafferentation on the reflex control of efferent renal sympathetic nerve activity (RSNA) in response to a stimulus that affected all vagal receptors in the cardiopulmonary region. METHODS AND RESULTS: Experiments were performed in 14 chloralose-anesthetized dogs with sinoaortic denervation. Reflex control of RSNA in response to blood volume expansion was measured before and after interruption of cardiac vagal afferents by pericardial lidocaine (PL). Reflex sensitivity (% change in RSNA/mm Hg change in left atrial pressure) was markedly attenuated after PL (pre, -10.9+/-2.2; post, -1.6+/-0. 6; P=0.002). RSNA responses to intracoronary nicotine and left atrial balloon inflation were abolished after PL, confirming that cardiac afferents were interrupted. RSNA responses to lung inflation were not affected by PL, indicating that pulmonary afferents remained intact. In 8 experiments, reflex sensitivity values returned to baseline levels after the effects of PL had worn off. CONCLUSIONS: These results indicate that the heart provides the primary source of afferent input for the control of sympathetic outflow by the vagal cardiopulmonary reflex during changes in thoracic blood volumes and pressures.
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Anthony J. Minisi (1998) studied this question. Interruption of cardiac vagal afferents by pericardial lidocaine vs. Before interruption (baseline) was evaluated on Reflex sensitivity (% change in RSNA/mm Hg change in left atrial pressure) (p=0.002). Interruption of cardiac vagal afferents by pericardial lidocaine markedly attenuated reflex sensitivity of renal sympathetic nerve activity (-1.6 vs -10.9 pre-intervention; P=0.002).
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