Effects of prior hypoxia exposure, endotoxin and sleep state on arousal ability to airway obstruction in piglets: implications for sudden infant death syndrome.

BACKGROUND: Respiratory tract infections may be an important component in many deaths attributed to sudden infant death syndrome (SIDS), although the mechanism of involvement remains unclear. OBJECTIVES: The hypothesis was tested that prolonged hypoxia and a thermogenic state (simulating a fever due to respiratory tract infection) would impair respiratory responsiveness to airway obstruction during sleep. METHODS: Thirty nine piglets aged 5-7 days were exposed to 24 h of moderate hypoxia and/or a low dose of endotoxin derived from Salmonella abortus equi. Responsiveness to complete and subtotal upper airway obstruction was tested during non-rapid eye movement (NREM) and rapid eye movement (REM) sleep. The end-point for airway obstruction tests was taken as the first protective response, either arousal or initiation of mouth breathing. Responsiveness was assessed as response time and response threshold (measured as respiratory effort, i.e. esophageal pressure swing). RESULTS: All animals demonstrated a thermogenic state following endotoxin delivery (drop in ear temperature of 5.8 +/- 0.2 degrees C and a small but significant increase in rectal temperature). Response time to subtotal airway obstruction was reduced during the heat conserving phase of the fever (thermogenesis; 2.8 +/- 0.5 s compared to 4.3 +/- 0.7 s during pre-endotoxin tests), but markedly increased during the recovery period (20.3 +/- 5.1 compared to 14.0 +/- 2.5 s pre-endotoxin) in NREM sleep. Response threshold was not significantly affected by either endotoxin or hypoxia in NREM sleep. Respiratory responsiveness to subtotal obstruction was markedly reduced during REM sleep (response time 40.3 +/- 10.9 s compared to 14.7 +/- 2.2 s in NREM; response threshold -14.0 +/- 1.3 mm Hg compared to -11.7 +/- 1.0 mm Hg in NREM). CONCLUSIONS: This study has demonstrated in a neonatal animal model that respiratory responsiveness to airways obstruction is delayed during recovery from fever. The findings may have implications for the human infant recovering from a respiratory illness.

Bed-sharing and the infant's thermal environment in the home setting.

AIMS: To study bed-sharing and cot-sleeping infants in the natural setting of their own home in order to identify differences in the thermal characteristics of the two sleep situations and their potential hazards. METHODS: Forty routine bed-sharing infants and 40 routine cot-sleeping infants aged 5-27 weeks were individually matched between groups for age and season. Overnight video and physiological data of bed-share infants and cot-sleeping infants were recorded in the infants' own homes including rectal, shin, and ambient temperature. RESULTS: The mean rectal temperature two hours after sleep onset for bed-share infants was 36.79 degrees C and for cot-sleeping infants, 36.75 degrees C (difference 0.05 degrees C, 95% CI -0.03 to 0.14). The rate of change thereafter was higher in the bed-share group than in the cot group (0.04 degrees C v 0.03 degrees C/h, difference 0.01, 0.00 to 0.02). Bed-share infants had a higher shin temperature at two hours (35.43 v 34.60 degrees C, difference 0.83, 0.18 to 1.49) and a higher rate of change (0.04 v -0.10 degrees C/h, difference 0.13, 0.08 to 0.19). Bed-sharing infants had more bedding. Face covering events were more common and bed-share infants woke and fed more frequently than cot infants (mean wake times/night: 4.6 v 2.5). CONCLUSIONS: Bed-share infants experience warmer thermal conditions than those of cot-sleeping infants, but are able to maintain adequate thermoregulation to maintain a normal core temperature.

Endotoxin effects on markers of autonomic nervous system function in the piglet: implications for SIDS.

The hypothesis was tested in 30 newborn piglets that the effects of a low dose of endotoxin (1 microg i.v. bolus; Salmonella abortus equi) would impair autonomic nervous system function. Two tests of autonomic function were performed following external warming (pre-endotoxin) and during endotoxin-generated thermogenesis: (1) analysis of heart rate variability in the time and frequency domains and (2) baroreflex sensitivity measured following intravenous injection of the vasoactive drugs nitroprusside and phenylephrine. Beat-to-beat heart rate variability (SDDeltaRR) fell by 2.2 ms from 7.0 ms before fever (p < 0.05). Low-frequency spectral power fell by 2.4 ms(2) from 4.1 ms(2) before fever (p < 0.05). The sensitivity of the baroreflex to changes in blood pressure induced by the vasoactive drugs decreased during fever by 0.72 ms/mm Hg for the nitroprusside test (p < 0.0005) and by 0.31 ms/mm Hg for the phenylephrine test (p < 0.005). These results indicate that in the piglet the balance of autonomic tone is altered and autonomic responsiveness reduced during the thermogenic phase of a fever. These findings are consistent with known risk factors for sudden infant death syndrome.

Respiratory responses to hypoxia/hypercapnia in small for gestational age infants influenced by maternal smoking.

AIM: To determine any variation in the respiratory responses to hypoxia/hypercapnia of infants born small for gestational age (SGA) to smoking and to non-smoking mothers. METHODS: A total of 70 average for gestational age (AGA) infants (>36 weeks gestation, >2500 g, >25th centile for gestational age, and no maternal smoking), and 47 SGA infants (<10th centile for gestational age) were studied at 1 and 3 months of age, in quiet and active sleep. Respiratory test gases were delivered through a Perspex hood to simulate face down rebreathing by slowly allowing the inspired air to be altered to a CO(2) maximum of 5% and O(2) minimum of 13.5%. The change in ventilation with inspired CO(2) was measured over 5-6 minutes of the test. The slope of a linear curve fit relating inspired CO(2) to the logarithm of ventilation was taken as a quantitative measure of ventilatory asphyxial sensitivity (VAS). RESULTS: There was no significant difference in VAS between the AGA and SGA infants (0.25 v 0.24). However within the SGA group, VAS was significantly higher (p = 0.048) in the infants whose mothers smoked during pregnancy (0.26 (0.01); n = 24) than in those that did not (0.23 (0.01); n = 23). The change in minute ventilation was significantly higher in the smokers than the non-smokers group (141% v 119%; p = 0.03) as the result of a significantly larger change in respiratory rate (8 v 4 breaths/min; p = 0.047) but not tidal volume. CONCLUSIONS: Maternal smoking appears to be the key factor in enhancing infants' respiratory responses to hypoxia/hypercapnia, irrespective of gestational age.

Prone versus supine sleep position: a review of the physiological studies in SIDS research.

A number of physiological studies, published over the last 10 years, have investigated the links between prone sleeping and sudden infant death syndrome (SIDS). This review evaluates those studies and derives an overview of the different affects of sleeping prone or supine in infancy. Generally, compared with the supine, the prone position raises arousal and wakening thresholds, promotes sleep and reduces autonomic activity through decreased parasympathetic activity, decreased sympathetic activity or an imbalance between the two systems. In addition, resting ventilation and ventilatory drive is improved in preterm infants, but in older infants (>1 month), there is no improvement in ventilation, and in 3-month-old infants, the position is adverse in terms of poorer ventilatory drive (in active sleep only). The majority of findings suggest a reduction in physiological control related to respiratory, cardiovascular and autonomic control mechanisms, including arousal during sleep in the prone position. Since the majority of these findings are from studies of healthy infants, continued reinforcement of the supine sleep recommendations for all infants is emphasized.