Investigating feed-forward neural regulation of circulation from analysis of spontaneous arterial pressure and heart rate fluctuations

Abstract

Background-Analysis of spontaneous fluctuations in systolic arterial pressure (SAP) and pulse interval (PI) reveals the occurrence of sequences of consecutive beats characterized by SAP and PI changing in the same (+PI/+SAP and -PI/-SAP) or opposite (-PI/+SAP and +PI/-SAP) direction. Although the former reflects baroreflex regulatory mechanisms, the physiological meaning of -PI/+SAP and +PI/-SAP is unclear. We tested the hypothesis that -PI/+SAP and +Pi/-SAP 'nonbaroreflex' sequences represent a phenomenon modulated by the autonomic nervous system reflecting a feed-forward mechanism of cardiovascular regulation. Methods and Results-We studied anesthetized rabbits before and after (1) complete autonomic blockade (guanethidine + propranolol + atropine, n = 13; CAB), (2) sympathetic blockade (guanethidine + propranolol, n = 15; SB), (3) parasympathetic blockade (atropine, n= 16), (4) sinoaortic denervation (n= 10; SAD), and (5) controlled respiration (n= 10; CR). Nonbaroreflex sequences were defined as ≥3 beats in which SAP and PI of the following beat changed in the opposite direction. CAB reduced the number of nonbaroreflex sequences (19.1 ± 12.3 versus 88.7 ± 36.6, P<0.05), as did SB (25.3±11.7 versus 84.6±23.9, P<0.001) and atropine (11.2±6.8 versus 94.1±32.4, P<0.05). SB concomitantly increased baroreflex sensitivity (1.18 ± 0.11 versus 0.47±0.09 ms/mm Hg, P<0.01). SAD and CR did not significantly affect their occurrence. Conclusions-These results suggest that nonbaroreflex sequences represent the expression of an integrated, neurally mediated, feed-forward type of short-term cardiovascular regulation able to interact dynamically with the feedback mechanisms of baroreflex origin in the control of heart period.