Kirjavainen, Turkka, Suvi Viskari, Olli Pitkänen, and Eero Jokinen. Infants with univentricular heart have reduced heart rate and blood pressure responses to side motion and altered responses to head-up tilt. J Appl Physiol 98: 518 -525, 2005; doi:10.1152/ japplphysiol.00248.2004.-Cardiovascular control was studied in infants with univentricular heart (UVH). Side motion tests and 45-s 45°h ead-up tilt tests were performed in 11 control and 9 UVH infants at the age of 13 Ϯ 3.2 wk. In addition, heart rate (HR) reactions to spontaneous arousals and HR variability during slow-wave sleep (SWS) were determined. All UVH infants had been hypoxic for several weeks, and during the sleep study the mean arterial oxyhemoglobin saturation was 82 Ϯ 5%. Tests were done at night during SWS, confirmed by polysomnographic recording. Continuous beatto-beat blood pressure (BP) was measured. In the side-motion tests, control infants consistently showed a transient increase in HR and BP. This response was markedly reduced in all of the UVH infants (P Ͻ 0.0001). In tilt tests, the UVH infants showed normal BP responses, but, although a sustained 2.0% decrease in HR was observed in the controls, the UVH infants presented with a sustained 2.6% mean HR increase (P ϭ 0.005). The UVH infants also showed attenuated HR acceleration during spontaneous arousals (P ϭ 0.01), but HR variability did not differ significantly from the controls. In conclusion, UVH infants with chronic hypoxia exhibit defective vestibulosympathetic pathways, as expressed by an absence of acute HR and BP reactivity to side motion. HR reactions to postural challenge and spontaneous arousal are also altered. Autonomic function abnormalities in these infants are suggested to be secondary to hypoxia. autonomic function; heart defects; congenital; hypoxia; sudden infant death SYSTEMIC BLOOD PRESSURE (BP) control is a complex process, with a multitude of input signals improving the accuracy of the regulatory system. Long-term absence of one type of signal does not fundamentally alter BP control, but acute control becomes more inaccurate (24,32,37,43). Cardiovascular reactions to postural challenge are known to be mediated by baroreflexes, peripheral venous reflexes, and vestibular sympathoreflexes (32,36,45). The orthostatic cardiorespiratory response is primarily mediated by the baroreflex. However, it takes 7-9 s for baroreceptors to induce substantial BP response to head-up tilt (34,39). Thus the baroreflex alone would be too slow to maintain adequate BP during rapid rises or sudden body movements. Fast responses to postural challenges are known to be induced by vestibular action, but the vestibular system also helps to maintain orthostatic reflexes (6, 43). Vestibular nuclei and cerebellar structures, especially the rostral part of the fastigial nucleus, are important in BP control during movements and hazardous situations such as hypovolemia and endotoxin shock (6, 28). Failure of the vestibular and cerebellar heart rate (HR) and BP compensation in hazardous situations ...

Vestibulo-mediated cardiovascular control in hazardous situations is important. Our hypothesis is that the prerequisite for sudden infant death syndrome (SIDS) is impaired vestibulo-mediated cardiovascular control. Prematurity is a risk factor for SIDS, and postnatal intermittent hypoxia may contribute to this risk. We studied heart rate (HR) and blood pressure (BP) responses in 10 infants with bronchopulmonary dysplasia (BPD) who were born at 27 Ϯ 2.4 (23-30) wk of gestation. Twenty healthy term infants served as controls. Cardiovascular tests were performed under polysomnographic control during slow-wave sleep (SWS) at a corrected age of 12 Ϯ 3.5 (7-19) wk. Control infants showed biphasic HR and BP responses to side motion with an immediate increase followed by a modest decrease and return to baseline. Compared with the controls, half of the BPD infants had altered BP responses (p Ͻ 0.005) without an early increase, followed by a more prominent decrease in BP. BPD infants also presented with a greater variability in BP responses to head-up tilts than did the controls (p Ͻ 0.001). In conclusion, these findings suggest that some BPD infants have impaired vestibular sympathoreflex-mediated cardiovascular control. This dysfunction may become critical in life-threatening situations. V estibular and cerebellar dysfunction has been suggested to be part of the pathophysiology of SIDS (1). Cardiovascular control mediated by vestibular nuclei and the cerebellum are important in hazardous situations such as hypovolemic and endotoxin shock (2,3). More than 80% of SIDS victims have shown neuronal apoptosis in vestibular nuclei and nuclei of the tractus solitarii, which are involved in baroand vestibular sympathoreflexes (4). SIDS victims also present with abnormalities elsewhere in the vestibular sympathoreflex pathway (5-7).During normal daily living, vestibular sympathoreflex dysfunction is not expected to have a profound effect on cardiovascular control because several compensatory circuits are involved in control of HR and BP (8,9). The dysfunction results in greater variability in BP control during postural changes (10). Similarly, increased BP variability has been observed in tilt tests performed in infants who have suffered from apparent life-threatening events (ALTEs) (11,12), further supporting the idea of vestibular dysfunction in SIDS.Most SIDS victims have suffered from hypoxia for at least several hours before the lethal event (13). SIDS victims may also have suffered from hypoxia earlier in life for multiple reasons, including placental insufficiency (14), intrauterine nicotine exposure (15), low or very low birth weight (16,17), hypoxia related to obstructive apnea events (18,19), or unfavorable head position during sleep (20,21). Our hypothesis is that hypoxic episodes cause a dysfunction in vestibulo-mediated cardiovascular control, thus making the infant more liable to die in life-threatening situations. To test the possible effects of hypoxia and test our hypothesis, we previously studied infan...