Fundamental relationships between arterial baroreflex sensitivity and dynamic cerebral autoregulation in humans

Tzeng YC, Lucas SJ, Atkinson G, Willie CK, Ainslie PN. Fundamental relationships between arterial baroreflex sensitivity and dynamic cerebral autoregulation in humans. J Appl Physiol 108: 1162-1168, 2010. First published March 11, 2010; doi:10.1152/japplphysiol.01390.2009.-The functional relationship between dynamic cerebral autoregulation (CA) and arterial baroreflex sensitivity (BRS) in humans is unknown. Given that adequate cerebral perfusion during normal physiological challenges requires the integrated control of CA and the arterial baroreflex, we hypothesized that between-individual variability in dynamic CA would be related to BRS in humans. We measured R-R interval, blood pressure, and cerebral blood flow velocity (transcranial Doppler) in 19 volunteers. BRS was estimated with the modified Oxford method (nitroprusside-phenylephrine injections) and spontaneous low-frequency (0.04-0.15) alpha-index. Dynamic CA was quantified using the rate of regulation (RoR) and autoregulatory index (ARI) derived from the thigh-cuff release technique and transfer function analysis of spontaneous oscillations in blood pressure and mean cerebral blood flow velocity. Results show that RoR and ARI were inversely related to nitroprusside BRS [R = -0.72, confidence interval (CI) -0.89 to -0.40, P = 0.0005 vs. RoR; R = -0.69, CI -0.88 to -0.35, P = 0.001 vs. ARI], phenylephrine BRS (R = -0.66, CI -0.86 to -0.29, P = 0.0002 vs. RoR; R = -0.71, CI -0.89 to -0.38, P = 0.0001 vs. ARI), and alpha-index (R = -0.70, CI -0.89 to -0.40, P = 0.0008 vs. RoR; R = -0.62, CI -0.84 to -0.24, P = 0.005 vs. ARI). Transfer function gain was positively related to nitroprusside BRS (R = -0.62, CI 0.24-0.84, P = 0.0042), phenylephrine BRS (R = 0.52, CI 0.10-0.79, P = 0.021), and alpha-index (R = -0.69, CI 0.35-0.88, P = 0.001). These findings indicate that individuals with an attenuated dynamic CA have greater BRS (and vice versa), suggesting the presence of possible compensatory interactions between blood pressure and mechanisms of cerebral blood flow control in humans. Such compensatory adjustments may account for the divergent changes in dynamic CA and BRS seen, for example, in chronic hypotension and spontaneous hypertension.