Cardiac sympathetic afferent sensitivity is enhanced in heart failure.

A previous study from this laboratory has shown that cardiac sympathetic afferent stimulation by epicardial application of bradykinin (BK) and capsaicin was significantly enhanced in the dog with experimental heart failure (HF). 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 from the left cardiac sympathetic nerve was recorded. Baseline cardiac sympathetic afferent discharge rate (spikes/s) and its responses to intra-atrial injection of BK were compared between sham and HF groups. Baseline cardiac sympathetic afferent discharge rate 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 sympathetic afferent responses to left intra-atrial injection of bradykinin (2 and 5 microgram/kg) and capsaicin (5 and 10 microgram/kg) were also significantly augmented. The sensitized cardiac sympathetic afferent responses to BK (2 and 5 microgram/kg, left intra-atrial injection) in the HF group were significantly reduced by the cyclooxygenase inhibitor indomethacin (5 mg/kg iv). The sensitized cardiac sympathetic afferent response to capsaicin (5 and 10 microgram/kg, left intra-atrial injection) in the HF group was preserved. It is suggested that the cardiac sympathetic chemosensitive afferent sensitivity is significantly enhanced in dogs with HF even though the baseline cardiac sympathetic afferent discharge is elevated.