Background: Baroreflex regulates arterial pressure (AP) via controlling sympathetic nerve activity (SNA). Baroreflex-controlled SNA is a powerful regulator of stressed blood volume, which, in turn, determines ventricular preload. We previously reported that baroreflex failure impaired the volume tolerance and markedly increased the variability of left atrial pressure (LAP) in normal rats. We hypothesized that, in chronic heart failure (CHF), baroreflex failure would further augment LAP variability and predispose to pulmonary edema.
Methods: Four weeks after creating myocardial infarct (MI) in Sprague-Dawley rats, we induced baroreflex failure by sino-aortic denervation (SAD). Two weeks after SAD, AP and LAP were measured telemetrically, low-pass filtered with the corner frequency of 0.4 Hz and resampled at 1 Hz. We compared the mean and variability (standard deviation, SD) of resampled AP and LAP among 3 groups; normal (Control, n=4), post-MI CHF (CHF, n=5) (left ventricular ejection fraction; LVEF 31.5 ± 1.4%), and CHF with SAD (CHF+SAD, n=5) (LVEF 31.6 ± 4.8 %).
Results: Mean AP (mAP) did not differ among 3 groups and SD of AP (SDAP) was significantly higher in CHF+SAD than in CHF (9.1 ± 1.1 vs. 6.5 ± 0.9 mmHg, p < 0.05) (Fig. 1). Mean LAP (mLAP) and SD of LAP (SDLAP) were significantly higher in CHF than in Control (mLAP: 27.2 ± 5.6 vs. 6.8 ± 0.7 mmHg, p < 0.01, SDLAP: 3.7 ± 0.6 vs. 2.0 ± 0.1 mmHg, p < 0.01). In CHF+SAD, SDLAP further increased (6.9 ± 1.5 mmHg, p < 0.05, vs. CHF) whereas mLAP remained unchanged (27.1 ± 3.6 mmHg, N.S.) (Fig. 2, 3). The duration of LAP higher than 35 mmHg (estimated threshold to cause pulmonary edema) markedly increased in CHF+SAD compared to CHF (21.5 ± 4.3 vs. 1.9 ± 1.4% of 24-h, p < 0.01) (Fig. 4).
Conclusions: Baroreflex failure increased spontaneous LAP variability in CHF rats and strikingly increased the duration of LAP>35 mmHg. Baroreflex failure may serve as a triggering mechanism as well as substrates of acute pulmonary edema in patients with CHF.