Abstract 16220: Baroreflex Failure Predisposes to Pulmonary Edema In Conscious Rats with Normal Left Ventricular Function
Backgrounds: In heart failure with preserved ejection fraction (HFPEF), diastolic dysfunction was the central dogma. However, recent investigations have indicated that the complex mechanisms are involved in the pathogenesis of HFPEF. The risk factors of HFPEF include ageing, hypertension, and chronic kidney disease. Those risk factors are in common with ordinary atherosclerosis. The sclerotic arteries are known to have lower baroreceptor transduction gain than physiological baroreceptors. Since the baroreflex buffers volume stress, we hypothesized that abolishing the baroreflex results in striking volume intolerance and predisposes to pulmonary edema even in the absence of left ventricular dysfunction.
Methods: In freely moving 5 Sprague-Dawley rats weighing 500±31g, we implanted a telemetry system to measure arterial pressure (AP) and left atrial pressure (LAP) and let them recovered at least for a week prior to sinoaortic denervation (SAD). AP and LAP were recorded for 24 hours a day before (Control) and 7 days after SAD.
Results: The mean values of AP and LAP were not significantly different between before and after SAD (AP: 103.9 ± 5.8 vs. 104.7 ± 6.1 mmHg, LAP: 7.0 ± 1.7 vs. 7.8 ± 2.0 mmHg), but their standard deviations (SD) were markedly increased after SAD (AP (left panel of Fig): 8.7 ± 1.0 vs. 16.5 ± 2.1 mmHg, LAP (middle panel of Fig): 1.83 ± 0.45 vs. 2.95 ± 0.65 mmHg, p < 0.05). As a result, the period of LAP>18 mmHg in 24 hours are markedly increased (4.2 ± 6.7 vs. 935 ± 868 sec, p < 0.05, the right panel of Fig).
Conclusions: Baroreflex failure does not change mean AP or LAP. However, baroreflex failure nearly doubled the variability of AP and LAP, and elevated LAP above 18 mmHg for nearly 15 min/day. Baroreflex failure predisposes to pulmonary edema in the absence of left ventricular dysfunction. Baroreflex failure may play a crucial role in the pathogenesis of HFPEF.
- © 2012 by American Heart Association, Inc.