Acute intermittent hypoxia (AIH) is a frequently studied experimental model of obstructive sleep apnoea (OSA). AIH can elicit a long-term increase in sympathetic outflow (long-term facilitation, LTF). Most investigators study AIH in mechanically ventilated, bilaterally vagotomised, and anesthetized animals. Under these conditions, the effect of AIH on the para-sympathetic nervous system (e.g. heart rate) cannot be observed. We hypothesized that heart rate change after AIH would also be regulated by LTF of vagus nerve activity. In urethane-anaesthetized, mechanically ventilated Sprague-Dawley rat, we investigated the effect of ten 45 s episodes of 10% O₂-90% N₂ on the heart rate and blood pressure change. We then tested whether or not hypoxic chemoreceptor reflex were changed 60 min after AIH. In bilaterally vagotomised animal preparations (n=7), we found that no animal manifested changes in heart rate compared with the time controls (rats not exposed to hypoxia, n=5). However, in vagally intact preparations (n=7), heart rate gradually increased by 28±7 beats per min at 60 minute after the last hypoxic episode (compared with time controls, n=4; P < 0.01). No mean arterial blood pressure changes were observed in either preparation. The increase in heart rate after hypoxia was enhanced after AIH in the vagally intact preparation (peak increase from 49±8 to 77±13 beats per min, n=7; P < 0.05). Also the decrease in mean arterial blood pressure during brief hypoxia was attenuated (from -47±3 to -32±5 mmHg, n=7; P < 0.05). No such changes were determined in the vagotomised preparations. These data suggests that AIH induces a long-term decrease of vagal innervation to the heart. The acute haemodynamic responses to hypoxia may indicate a neurocirculatory adaption to chemoreflex control systems by vagal parasympathetic neurons following AIH. The changes observed may be important in the pathophysiology of OSA.