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Pulmonary stretch receptor afferents inhibit sympathetic nerve activity in early heart failure.
Author(s) -
Dick Thomas E,
Wang Ning,
Liner Anna,
Hoit Brian D
Publication year - 2007
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.21.6.a1269-c
Subject(s) - medicine , expiration , phrenic nerve , hypoxia (environmental) , anesthesia , microneurography , heart failure , cardiology , oxygenation , vagus nerve , respiratory system , endocrinology , heart rate , chemistry , blood pressure , stimulation , oxygen , baroreflex , organic chemistry
Continuous positive airway pressure (CPAP) reduces sympathetic nerve activity (SNA) in patients with heart failure (HF). We tested the hypothesis that reduction of SNA with CPAP in HF results from increased sensitivity to pulmonary afferents. Sprague‐Dawley adult male rats underwent coronary artery ligation (Group 1, n=8) or sham surgery (Group 2, n=9) and were followed by serial echocardiograms. At 18 wks, Group 1 was in early HF. Then we anesthetized animals and recorded phrenic and splanchnic sympathetic nerve activities (PNA & sSNA). A cycle‐triggered pump coordinated lung inflation with PNA. Cycle‐triggered averages of sSNA were generated to determine the relationship of sSNA to respiration. Animals were exposed to brief hypoxia (8%, 45s) to recruit sSNA. In sham animals, hypoxia‐evoked sSNA during expiration and inhibited it during inspiration. This coupling pattern occurred only after transecting the vagus in animals with early HF. We conclude that in early HF, vagal afferent activity shapes sSNA by decreasing activity during expiration and that these effects are particularly prominent during hypoxia in early HF. Thus, CPAP decreases SNA in HF patients by not only improving oxygenation but also directly inhibiting SNA via activation of vagal afferents. NIH HL080318