Effect of Maturation on Heart Rate Response to Ocular Compression Test during Rapid Eye Movement Sleep in Human Infants

Ramet, José; Praud, Jean‐Paul; Am, D'Allest; Carofilis, A; Dehan, M; Guilleminault, Christian; Gaultier, C

doi:10.1203/00006450-198810000-00012

Cited by 29 publications

(25 citation statements)

References 9 publications

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“…States of alertness exert a pro found influence on autonomic mechanisms controlling heart rate and heart rate variabili ty [9], Differences observed in adults suggest that the sympathetic activity predominates during rapid eye movement (REM) sleep and the parasympathetic activity during non-REM (NREM) sleep [10,11]. Similar differ ences in heart rate control between sleep states have been documented early in human ontogenesis [12], We previously studied the effects of maturation in healthy infants or heart rate response to ocular compression [13], a maneuver that elicits a well-known vagally mediated reflex [14]. In the present study, we investigated whether states of alert ness influence heart rate response to this pha sic vagal stimulus in infants.…”

Section: Introductionmentioning

confidence: 91%

Effect of State of Alertness on the Heart Rate Response to Ocular Compression in Human Infants

Ramet

Hauser²,

Dehan³

et al. 1995

Neonatology

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Because the state of alertness exerts a profound influence on autonomic cardiac control, we hypothesized, that the heart rate response to a vagal stimulus, i.e., ocular compression, may differ during different states of alertness. We studied 8 healthy infants with a postconceptional age of 35-41 weeks (mean ± SD 37.9 ± 2.1 weeks). They underwent a standardized ocular compression test during polygraphically controlled wakeful-ness, rapid eye movement (REM) sleep, and non-REM (NREM) sleep. The R-R intervals were measured (1) during the 60 s preceding the ocular compression test, to determine the mean control R-R interval, and (2) during compression. Percent R-R interval was defined as the longest R-R interval in milliseconds during the test divided by the mean control R-R interval and multiplied by 100. The longest R-R interval during the test was significantly greater in REM sleep than in wakefulness (p < 0.05) and in NREM sleep (p < 0.01): 939 ± 360, 623 ± 355, and 538 ± 60 ms, respectively. The percent R-R interval was significantly greater in REM sleep than in NREM sleep (p < 0.01): 236 ± 91 and 129 ± 16, respectively. The time from the longest R-R interval to return to mean control R-R interval, i.e., vagal escape, was significantly shorter in REM sleep than in NREM sleep and in wakefulness (p < 0.01): 843 ± 168,2,131 ± 712, and 2,078 ± 913 ms, respectively. This study indicates that the state of alertness should be defined when performing tests on autonomic reflexes in infants.

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Section: Introductionmentioning

confidence: 91%

Effect of State of Alertness on the Heart Rate Response to Ocular Compression in Human Infants

Ramet

Hauser²,

Dehan³

et al. 1995

Neonatology

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“…Infants born preterm may eventually catch up to their counterparts born at term, although to what extent presumably depends on whether key events occur at the proper time and in the correct sequence, e.g. changes in baroreflex control (which normally strengthens), cardiovagal inhibition (which weakens), metabolism (which slowly decreases), vascular resistance (which increases), and within the heart itself (27,42,43). Because the HR of the preterm infant is often elevated at 6 mo, central and peripheral mechanisms involved in cardiac (and perhaps circulatory) control may be quite slow to reset or normalize (if at all) (44).…”

Section: Discussionmentioning

confidence: 99%

Abnormal Circulatory Stress Responses of Preterm Graduates

2007

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Preterm birth and chronic lung disease may increase the risk of hypertension and cardiovascular disease in infancy and adolescence. Here we looked for evidence of early circulatory dysfunction associated with these perinatal complications. We compared infants born at term (n ϭ 12) with those born preterm with an uncomplicated neonatal course (n ϭ 12) or diagnosed with bronchopulmonary dysplasia (BPD) (n ϭ 10). We measured blood pressure (BP) (Finometer), and heart rate (HR) responses to 4 min of breathing 4% CO 2 during quiet sleep. Hypercapnia accelerated HR and increased BP of term infants. Preterm infants either (i) had an exaggerated pressor but little or no HR response to CO 2 (healthy or mild-moderate BPD) or (ii) had a diminished pressor response and accompanying decrease in HR (severe BPD). Short-term reflex cardiovascular control was consequently altered by premature birth, with potentially more serious aberrations associated with severe BPD. Most anomalies had not resolved by the time infants born preterm reached term age; some may be early signs of emerging long-term cardiovascular dysfunction. W ith the impressive increase in survival of very preterm and low birth weight infants come new challenges. Evidence already indicates that this "new generation" of children and adolescents may have accelerated disease onset later in life (1). One factor contributing to their higher risk of cardiovascular disease may be abnormal vascular and circulatory development (2-4). Cardiovascular activity is normally carefully regulated, but if some or all of the central and peripheral regulatory mechanisms involved fail to develop normally, perfusion, growth, and function may be compromised. In exceptional circumstances during infancy, persistent serious dysfunction could result in a sudden catastrophic decrease in BP and HR or prevent autoresuscitative recovery, culminating in sudden infant death syndrome (SIDS) (5,6). In other cases, dysfunction may be relatively benign, although there may still be side effects with adverse consequences of their own.We know relatively little about how BP and HR control develops, and the potentially adverse effects of fetal and perinatal stress. A better understanding of these issues could lead to new therapies or strategies to prevent neonatal complications and improve long-term outcome. In the study described here, we looked for evidence that development of neonatal circulatory control is altered by common perinatal complications (7). We studied three different groups of newborn infants: those born normally at term, those born preterm but otherwise healthy, and infants born very preterm suffering from chronic lung disease (BPD). Infants with BPD are at particularly high risk of long-term cardiovascular complications and SIDS (8 -10). We compared BP and HR responses of these infants to a routine physiologic stress (breathing a low concentration of CO 2 for several minutes) commonly used to unmask autonomic anomalies (11). Normally, acute exposure to CO 2 increases BP and HR ...

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“…In active sleep no maturation in heart rate responses was observed in either preterm or term infants, however in quiet sleep the magnitude of the heart rate response increased with chronological age in both preterm and term infants (Tuladhar et al, 2005b). These findings are in contrast to other studies which have reported that the bradycardic reflex decreases with age after birth in both preterm and term infants in responses to trigeminal air-stream stimulation to the face, ocular compression and esophageal dilation and during active sleep and that by term responses were minimal (Ramet et al, 1995, Ramet et al, 1988, Ramet et al, 1990. The authors suggested that this bradycardic reflex may be inappropriate and increase the risk of the Sudden Infant Death Syndrome (SIDS) in preterm infants.…”

Section: Reflex Heart Rate Responsesmentioning

confidence: 58%