Arterial baroreflex impairment and functional plasticity of cardiac autonomic neurons in rat models of liver cirrhosis

Abstract

Background: Patients with heart failure with preserved ejection fraction (HFpEF) frequently suffer from pulmonary edema with little weight gain indicating underlying a volume supersensitive mechanism. We recently demonstrated that baroreflex failure resulted in striking volume intolerance. In this study, we examined how baroreflex failure impacts on daily fluctuations of left atrial pressure (LAP) in hypertensive rats. Methods: We allocated freely moving 14 weeks old spontaneously hypertensive rats (SHR) (n= 20) into 2 groups. We conducted sinoaortic denervation (SAD, n = 10) to abolish the baroreflex or sham operation (Sham, n= 10). In the following week, we implanted a telemetry system to measure arterial pressure (AP) and LAP. One week after the second surgery (16 weeks old), 2 groups were subjected to either normal (N-salt, 0.5% NaCl) or high salt diet (H-salt, 8% NaCl). We recorded 24-hours AP and LAP at a week after the initiation of N-salt or H-salt diet. Results: SAD significantly increased the standard deviations (SD) of AP both in N-salt and in H-Salt. In contrast, only SAD with H-salt increasedmean LAP (SAD/H-salt: 14.4 ± 2.3 vs. Sham/N-salt: 11.0 ± 1.5 mmHg, p b 0.05) with marked increases in their SDs (5.2 ± 0.6 vs. 1.3 ± 0.1 mmHg, p b 0.05). Furthermore SAD with H-salt strikingly prolonged the critically elevated LAP period (≧20 mmHg) by more than 20% of 24 hours. Conclusions: Baroreflex failure markedly increases daily fluctuations of LAP and prolongs the period of critically elevated LAP. Baroreflex failure induces volume intorelance and predisposes to pulmonary edema in hypertensive rats with high salt diet.