Remifentanil can cause bradycardia either by parasympathetic activation or by other negative chronotropic effects. The high frequency (HF) component of heart rate variability (HRV) is a marker of parasympathetic activity. This study aimed to evaluate the effect of remifentanil on RR interval and on HRV in children. Forty children ASA I or II were studied after approval by the human studies committee and informed parental consent was obtained. After stabilisation at sevoflurane 1 MAC, they were randomly divided into two groups: one received a 20 microg.kg(-1) atropine injection (AT + REMI) and the other ringer lactate solution (REMI). Three minutes later, a 1 microg.kg(-1) bolus of remifentanil was administered over 1 min, followed by a continual infusion at 0.25 microg.kg(-1).min(-1) for 10 min increased to 0.5 microg.kg(-1).min(-1) for a further 10 min. A time varying, autoregressive analysis of RR sequences was used to estimate classical spectral parameters: low (0.04-0.15 Hz; LF) and high (0.15-0.45 Hz; HF) frequency, whereas the root mean square of successive differences of RR intervals (rmssd) was derived directly from the temporal sequence. Statistical analyses were conducted by means of the multiple correspondence analysis and with non parametrical tests. Remifentanil induced an RR interval lengthening, i.e. bradycardia, in both groups compared to pretreatment values and was associated with an increase of HF and rmssd only for the REMI group. The parasympathetic inhibition by atropine did not totally prevent remifentanil's negative chronotropic effect. A direct negative chronotropic effect of remifentanil is proposed.