Abstract 1593: Activation of the Cardiac Sympathetic Afferent Reflex Enhances the Neuronal Chemosensitivity in the Nucleus Tractus Solitarius in Rats with Chronic Heart Failure
The cardiac sympathetic afferent reflex (CSAR) has been reported to play an important role in sympathetic overactivity as well as in the peripheral chemoreflex enhancement in the chronic heart failure (CHF). However, the exact mechanisms responsible for the interaction between the CSAR and chemoreflex function are poorly understood. It is well known that the nucleus tractus solitarius (NTS) is an essential region to effectively modulate cardiovascular reflexes. Hence, the present study was designed to test the hypothesis that the NTS contributes to the processing of the interaction between the CSAR and the chemoreflex in CHF at the level of chemosensitive neurons. CHF was produced by coronary artery ligation. In anesthetized and paralyzed sham and CHF rats a total of 52 spontaneously discharging neurons (resting discharge: 6.1 ± 0.8 spikes/sec) were recorded and functionally identified for peripheral chemosensitivity by intra-carotid injection of potassium cyanide (20 μg). In 28 neurons from CHF rats, CSAR activation by epicardial application of capsaicin (0.4 μg) not only significantly excited the baseline activity by 57.3 ± 7.5% (P<0.01) but also increased the neuronal chemosensitivity by 64.6 ± 5.9% (P<0.01). In 16 units from sham rats, the magnitude of the increase in resting activity was 36.5 ± 5.8% and neuronal chemosensitivity was increased by 41.9 ± 7.8% evoked by epicardial capsaicin. This was significantly lower (P<0.01) than that from CHF rats. Furthermore, in the remaining 8 units from CHF rats, tonic blockade of the cardiac sympathetic afferent input by epicardial application of lidocaine (2% in 6 μl) significantly (P<0.01) attenuated the neuronal chemosensitivity by 38.1 ± 7.1%. In conclusion, the current results suggest that the NTS mediates the peripheral chemoreflex enhancement evoked by CSAR activation in CHF.