a previous study from this laboratory has shown that cardiac sympathetic af
ferent stimulation by epicardial application of bradykinin (BK) and capsaic
in was significantly enhanced in the dog with experimental heart failure (H
F). The present study determined whether activity from cardiac sympathetic
chemosensitive afferent endings is enhanced in HF. Rapid ventricular pacing
was induced in six dogs; Five sham dogs served as controls. At the time of
the acute experiment, the dogs were anesthetized with pentobarbital sodium
(30 mg/kg iv). A thoracotomy was performed in the second intercostal space
, and single afferent fiber discharge fi om the left, cardiac sympathetic n
erve was recorded. Baseline cardiac sympathetic afferent discharge rate (sp
ikes/s) and its responses to intra-atrial injection of BK were compared bet
ween sham and HF groups. Baseline cardiac sympathetic afferent discharge ra
te in the HF group was significantly elevated compared with the sham group
(4.3 +/- 0.5 vs. 2.2 +/- 0.6 spikes/s, P < 0.05). In addition, cardiac symp
athetic afferent responses to left intra-atrial injection of bradykinin (2
and 5 mu g/kg) and capsaicin (5 and 10 mu g/kg) were also significantly aug
mented. The sensitized cardiac sympathetic afferent responses to BK (2 and
5 mu g/kg, left intra-atrial injection) in the HF group were significantly
reduced by the cyclooxygenase inhibitor indomethacin (5 mg/kg iv). The sens
itized cardiac sympathetic afferent response to capsaicin (5 and 10 mu g/kg
, left intra-atrial injection) in the HF group was preserved. It is suggest
ed that the cardiac sympathetic chemosensitive afferent sensitivity is sign
ificantly enhanced in dogs with HF even though the baseline cardiac sympath
etic afferent discharge is elevated.