Abstract 13356: Effects of Chronic Vagal Stimulation on Open-loop Baroreflex Function in Heart Failure Rats
Background: Vagal nerve stimulation (VNS) is explored as a new treatment for chronic heart failure (CHF). Although arterial baroreflex function is known to be depressed in CHF, effects of the VNS treatment on the open-loop characteristics of the arterial baroreflex remain unknown. The present study aimed to quantify the effects of the VNS treatment on the baroreflex function in CHF rats.
Methods: Myocardial infarction was produced in anesthetized rats. The rats survived after myocardial infarction was implanted with a telemetry transmitter for blood pressure monitoring and a radio stimulator for VNS. The right vagal nerve was chronically stimulated (10 seconds per minute). After 6 weeks of VNS treatment, the rat was anesthetized and the carotid sinus baroreceptor regions were isolated from the systemic circulation. The aortic depressor nerves and the vagi were sectioned bilaterally. The isolated carotid sinuses were exposed to a staircase-wise pressure input from 60 to 180 mmHg with an increment of 20 mmHg per minute. Changes in sympathetic nerve activity (SNA) and arterial pressure (AP) in response to baroreceptor pressure input were compared between VNS-treated (n = 7) and untreated (n = 7) CHF rats.
Results: The maximum percent SNA reduction was significantly greater in the VNS-treated than in the untreated group (59.6±5.4% vs. 34.8±8.3%, P = 0.027), suggesting improved baroreflex function to suppress SNA. In contrast, the slope of the AP response to a percent increase in SNA was not significantly different between the VNS-treated and untreated groups (0.65±0.08 vs. 0.73±0.05 mmHg/%, P = 0.42). There was no statistically significant difference in the response range of AP (41.2±0.7 vs. 26.7±6.1 mmHg, P = 0.15) or the maximum gain of the AP regulation (1.53±0.42 vs. 0.92±0.21, P = 0.21) between the two groups.
Conclusion: Chronic VNS treatment improved the arterial baroreflex function to suppress SNA, but the improvement of the overall function to regulate AP was limited due to the lack of significant improvement of the AP response to a percent increase in SNA.
- © 2013 by American Heart Association, Inc.