A. Cevese et al., Baroreflex and oscillation of heart period at 0.1 Hz studied by alpha-blockade and cross-spectral analysis in healthy humans, J PHYSL LON, 531(1), 2001, pp. 235-244
1. Parameters derived from frequency-domain analysis of heart period and bl
ood pressure variability are gaining increasing importance in clinical prac
tice. However, the underlying physiological mechanisms in human subjects ar
e not fully understood. Here we address the question as to whether the low
frequency variability (similar to0.1 Hz) of the heart period may depend on
a baroreflex-mediated response to blood pressure oscillations, induced by t
he alpha -sympathetic drive on the peripheral resistance.
2. Heart period (ECG), finger arterial pressure (Finapres) and respiratory
airflow were recorded in eight healthy volunteers in the supine position wi
th metronome respiration at 0.25 Hz. We inhibited the vascular response to
the sympathetic vasomotor activity with a peripheral alpha -blocker (urapid
il) and maintained mean blood pressure at control levels with angiotensin I
I.
3. We performed spectral and cross-spectral analysis of heart period (nn) a
nd systolic pressure to quantify the power of low- and high-frequency oscil
lations, phase shift, coherence and transfer function gain.
4. In control conditions, spectral analysis yielded typical results. In the
low-frequency range, cross-spectral analysis showed high coherence (>0.5)
and a negative phase shift (-65.1 +/- 18 deg) between RR and systolic press
ure, which indicates a 1-2 s lag in heart period changes in relation to pre
ssure. In the high-frequency region, the phase shift was close to zero, ind
icating simultaneous fluctuations of RR and systolic pressure. During urapi
dil + angiotensin II infusion the low-frequency oscillations of both blood
pressure and heart period were abolished in five cases. In the remaining th
ree cases they were substantially reduced and lost their typical cross-spec
tral characteristics.
5. We conclude that in supine rest conditions, the oscillation of nn at low
frequency is almost entirely accounted for by a baroreflex mechanism, sinc
e it is not produced in the absence of a 0.1 Hz pressure oscillation.
6. The results provide physiological support for the use of non-invasive es
timates of the closed-loop baroreflex gain from cross-spectral analysis of
blood pressure and heart period variability in the 0.1 Hz range.