Donate Help Contact The AHA Sign In Home
American Heart Association
Circulation
Search: search_blue_button Advanced Search
Circulation. 1998;98:2615-2620

This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow Request Permissions
Citing Articles
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Minisi, A. J.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Minisi, A. J.

(Circulation. 1998;98:2615-2620.)
© 1998 American Heart Association, Inc.


Basic Science Reports

Vagal Cardiopulmonary Reflexes After Total Cardiac Deafferentation

Anthony J. Minisi, MD

From the Department of Internal Medicine (Cardiology), Medical College of Virginia/Virginia Commonwealth University and Hunter Holmes McGuire Department of Veterans Affairs Medical Center, Richmond.

Correspondence to Anthony J. Minisi, MD, Cardiology Section (111J1), McGuire VA Medical Center, 1201 Broad Rock Blvd, Richmond, VA 23249. E-mail minisi.anthony_j.{at}richmond.va.gov

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.


Key Words: nervous system, autonomic • nervous system, sympathetic • lidocaine