Abstract 8890: Artificial Baroreceptor Fully Antagonizes Baroreflex Failure Induced Volume Intolerance
Backgrounds: Patients with heart failure with preserved ejection fraction have severe atherosclerosis and thereby baroreflex failure resulting from stiffened baroreceptors. We demonstrated that baroreflex failure induces striking volume intolerance and predisposes to pulmonary edema irrespective of left ventricular (LV) function. At present, however, there is no treatment for baroreceptor failure. The aim of this study is to develop artificial baroreceptor (ABaro) to restore physiological volume buffering function.
Methods: We vascularily isolated the baroreceptor regions in 14 Sprague-Dawley rats. The intra-carotid sinus pressure (CSP) was controlled by a servo-controlled pump. We randomly perturbed CSP and identified the transfer function from CSP to arterial pressure (AP). We randomly, electrically stimulated aortic depressor nerves (ADN) and identified the transfer function from ADN stimulation to AP. Taking the ratio of those two transfer functions yielded the transfer function (HABS) required for the ABaro. ABaro translates AP real-time to ADN stimulation according to HABS. We implemented ABaro and observed the left atrial pressure (LAP) response against stepwise infusions of dextran (Fig. 1). ABaro fully restored the physiological LAP-infused volume relationship (Fig. 2) and markedly increased the infused volume required to raise LAP to 20 mmHg (native: 20.1±3.2, baroreflex failure: 16.6±4.4, ml/kg ABaro: 21.0±3.0 ml/kg).
Conclusion: ABaro reinstitutes the native baroreflex and would be an attractive tool in preventing pulmonary edema in patients with poor baroreceptor function irrespective of LV systolic function.
- © 2011 by American Heart Association, Inc.