Influence of the thermal environment on HRV parameters calculated from the Poincaré plot.

<p>Mean values (± s.d.) of (A) SD1 and SD2 and (B) the cardiac vagal index and cardiac sympathetic index in the cool condition (T_N-2°C), at thermoneutrality (T_N) and in the warm condition (T_N+2°C) during active sleep (empty bars) and quiet sleep (black bars). * <i>P</i><0.05; ** <i>P</i><0.01; *** <i>P</i><0.001.</p

Frequency-domain HRV parameters in the cool condition (T_N-2), at thermoneutrality (T_N) and in the warm condition (T_N+2) during active sleep (AS) and quiet sleep (QS).

<p>Values are quoted as the mean ± standard deviation. NS: non-significant in an analysis of variance with repeated measures.</p

Heart Rate Variability in Sleeping Preterm Neonates Exposed to Cool and Warm Thermal Conditions

<div><p>Sudden infant death syndrome (SIDS) remains the main cause of postneonatal infant death. Thermal stress is a major risk factor and makes infants more vulnerable to SIDS. Although it has been suggested that thermal stress could lead to SIDS by disrupting autonomic functions, clinical and physiopathological data on this hypothesis are scarce. We evaluated the influence of ambient temperature on autonomic nervous activity during sleep in thirty-four preterm neonates (mean ± SD gestational age: 31.4±1.5 weeks, postmenstrual age: 36.2±0.9 weeks). Heart rate variability was assessed as a function of the sleep stage at three different ambient temperatures (thermoneutrality and warm and cool thermal conditions). An elevated ambient temperature was associated with a higher basal heart rate and lower short- and long-term variability in all sleep stages, together with higher sympathetic activity and lower parasympathetic activity. Our study results showed that modification of the ambient temperature led to significant changes in autonomic nervous system control in sleeping preterm neonates. The latter changes are very similar to those observed in infants at risk of SIDS. Our findings may provide greater insight into the thermally-induced disease mechanisms related to SIDS and may help improve prevention strategies.</p></div

Sleep structure parameters when given a choice between three air temperatures values.

<p>Mean ± SEM values for the different sleep stages in the control and the RF-EMF-exposed groups when given a choice between 24°C, 28°C and 31°C during light and dark periods and during 24 h periods. Amounts are in fact expressed as a percentage of the analysis time, which due to animal caring, is less than 24 h. Statistically significant differences between the control and exposed groups are indicated as follows: (*): p<0.05 and (**): p<0.01.</p

Heart rate and time-domain HRV parameters in the cool condition (T_N-2°C), at thermoneutrality (T_N) and in the warm condition (T_N+2°C) during active sleep (AS) and quiet sleep (QS).

<p>Values are quoted as the mean ± standard deviation. NS: non-significant in an analysis of variance with repeated measures.</p

Sleep and ventilatory data in the cool condition (T_N-2°C), at thermoneutrality (T_N) and in the warm condition (T_N+2°C).

<p>Values are quoted as the mean ± standard deviation. NS: not significant.</p

Thermal photographs of a control rat and an exposed rat at air temperature of 31°C.

<p>The colors correspond to the temperature scale on the right.</p

Thermal preference for controls (A) and RF-EMF exposed rats (B) over a 24 h period.

<p>The mean ± SEM time (in minutes, averaged over two-hour periods) spent in each of the three air temperatures zones (24°C (•), 28°C (□) and 31°C (▴), indicating the preferred temperature) during the dark and light periods.</p

Effect of the period on normalized values (mean ± SEM) of the power spectra in the low- (LF_nu) and high-frequency (HF_nu) bands.

<p>*<i>P</i><0.05, **<i>P</i><0.01. (pairwise multiple comparison procedures were used to test the differences between the control, prior and during periods. Data were adjusted for multiple testing with the Tukey-Kramer test).</p

Impact of chronic exposure to the pesticide chlorpyrifos on respiratory parameters and sleep apnea in juvenile and adult rats

<div><p>The widely used organophosphorus pesticide chlorpyrifos (CPF) is often detected in food. CPF inhibits acetylcholinesterase and can modify muscle contractility and respiratory patterns. We studied the effects of chronic exposure to CPF on respiratory parameters and diaphragm contractility in 21- and 60-days old rats. Pregnant rats were exposed to oral CPF (1 or 5 mg/ kg /day: CPF-1 or CPF-5 groups vs vehicle: controls) from gestation onset up to weaning of the pups that were individually gavaged (CPF or vehicle) thereafter. Two developmental time points were studied: weaning (day 21) and adulthood (day 60). Whole-body plethysmography was used to score breathing patterns and apnea index during sleep. Then, diaphragm strips were dissected for the assessment of contractility and acetylcholinesterase activity. Results showed that the sleep apnea index was higher in CPF-exposed rats than in controls. In adult rats, the expiratory time and tidal volume were higher in CPF-exposed animals than in controls. At both ages, the diaphragm’s amplitude of contraction and fatigability index were higher in the CPF-5 group, due to lower acetylcholinesterase activity. We conclude that chronic exposure to CPF is associated with higher sleep apnea index and diaphragm contractility, and modifies respiratory patterns in sleeping juvenile and adult rats.</p></div