ABSTRACT. Little is known of the development of efficient coordination between suckle feeding and breathing in human infants. To establish baseline data, we recorded breathing and swallowing activity during bottle feeds in 23 infants at 14-48 h postnatal age. Most swallows (overall mean 68%) were organized into runs, with intervals starting at 0.6-0.8 s and slowing to 1-1.3 s after 30-40 s. The proportion of run swallows to total swallows increased significantly with age. Swallow intervals were regular (coefficient of variation = 18-38%) compared with breathing (coefficient of variation = 50%). Both breathing rate and tidal volume were significantly reduced by the onset of suckle feeding, and the pattern of respiratory airflow became markedly irregular. Mild transient desaturation was common, but was not accompanied by changes in heart rate. Swallows could occur in all phases of breathing. Overall, equal numbers of swallows were preceded by expiration and inspiration, but twice as many were followed by expiration compared with inspiration. Swallows were classified by the respiratory phases both preceding and following the swallow. Swallows occurred in all possible classifications in each of the infants studied. The incidence of the most frequent classification (inspiration-swallowexpiration), was 24% overall (individual range 5-50%). The phase relation between swallows and breaths changed frequently but showed occasional short periods of stability during which the breathing became regular and tidal volume increased. We conclude that at <48 h the normal infant has little coordination between swallowing and breathing rhythms and maintains rhythmic swallowing at the expense of eupnea. (Pediatr Res 31: 619-624,1992)

Abnormal central regulation of upper airway muscles may contribute to the pathophysiology of the childhood obstructive sleep apnea syndrome (OSAS). We hypothesized that this was secondary to global abnormalities of ventilatory control during sleep. We therefore compared the response to chemical stimuli during sleep between prepubertal children with OSAS and controls. Patients with OSAS aroused at a higher PCO2 (58 +/- 2 vs. 60 +/- 5 Torr, P < 0.05); those with the highest apnea index had the highest arousal threshold (r = 0.52, P < 0.05). The hypercapnic arousal threshold decreased after treatment. For all subjects, hypoxia was a poor stimulus to arousal, whereas hypercapnia and, particularly, hypoxic hypercapnia were potent stimuli to arousal. Hypercapnia resulted in decreased airway obstruction in OSAS. Ventilatory responses were similar between patients with OSAS and controls; however, the sample size was small. We conclude that children with OSAS have slightly blunted arousal responses to hypercapnia. However, the overall ventilatory and arousal responses are normal in children with OSAS, indicating that a global deficit in respiratory drive is not a major factor in the etiology of childhood OSAS. Nevertheless, subtle abnormalities in ventilatory control may exist.

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Regulation of arterial oxygen levels is critically important in mammals, particularly during early life. Peri-and postnatal hypoxia may lead to impaired cognitive development, abnormalities in cardiovascular function, breathing control maturation and lung function, and death (Okubo & Mortola, 1988;Nyakas et al. 1996;Hudlicka & Brown, 1996). The main sensors of arterial Oµ tension are the carotid body chemoreceptors, which are located bilaterally at the bifurcations of the common carotid arteries. Carotid chemoreceptor sensory afferents, via the carotid sinus nerves (CSN), project to the nucleus tractus solitarii and other brainstem nuclei, providing the major source of Oµ-mediated ventilatory drive. Neural signals from the carotid chemoreceptors to brainstem cardiorespiratory control nuclei also mediate critically important respiratory reflexes such as arousal from sleep during hypoxia and cardiovascular reflexes that modulate heart rate and blood pressure (Marshall, 1987). The primary site of oxygen sensing in the carotid body is thought to be the type I cell (Gonzalez et al. 1994). Type I cells are specialized sensory neurons which depolarize in response to low Oµ, resulting in Ca¥ entry via voltage-gated calcium channels, and exocytosis of neurotransmitters and modulators onto apposed CSN terminals (Gonzalez et al. 1994). Although further study is needed to define their precise role, there is little question that type I cells play a crucial role in carotid chemoreceptor oxygen sensing. Carotid denervation, which is well tolerated by adults, in neonates leads to profound abnormalities of respiratory control and high mortality rates. In piglets and in lambs the

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1. The microvasculature of the lung of the duck and pigeon was studied by scanning electron microscopy of vascular casts and critical point dried preparations of the gas exchange tissue. 2. The gas-exchange cappilaries are discrete tubular vessels intimately associated with air capillaries in a three dimensional network. 3. The capillaries originate from arteries at the periphery of the parabronchus, and are collected by veins which run close to its luminal surface. 4. The capillary bed of 3-5 atria is drained by a single vein. It is suggested that the vein and its associated capillaries may form a controllable subunit of pulmonary perfusion.

The site of postnatal maturation of carotid body chemoreception is unclear. To test the hypothesis that maturation occurs synchronously in type I cells and the whole carotid body, the development of changes in the intracellular Ca2+ concentration responses to hypoxia, CO2, and combined challenges was studied with fluorescence microscopy in type I cells and compared with the development of carotid sinus nerve (CSN) responses recorded in vitro from term fetal to 3-wk animals. Type I cell responses to all challenges increased between 1 and 8 days and then remained constant, with no multiplicative O2-CO2interaction at any age. The CSN response to hypoxia also matured by 8 days, but CSN responses to CO2 did not change significantly with age. Multiplicative O2-CO2interaction occurred in the CSN response at 2–3 wk but not in younger groups. We conclude that type I cell maturation underlies maturation of the CSN response to hypoxia. However, because development of responses to CO2 and combined hypoxia-CO2 challenges differed between type I cells and the CSN, responses to these stimuli must mature at other, unidentified sites within the developing carotid body.

The response to inspiratory resistance loading (IRL) of the upper airway during sleep in children is not known. We, therefore, evaluated the arousal responses to IRL during sleep in children with the obstructive sleep apnea syndrome (OSAS) compared with controls. Children with OSAS aroused at a higher load than did controls (23 +/- 8 vs. 15 +/- 7 cmH(2)O. l(-1). s; P < 0.05). Patients with OSAS had higher arousal thresholds during rapid eye movement (REM) vs. non-REM sleep (P < 0.001), whereas normal subjects had lower arousal thresholds during REM (P < 0.005). Ventilatory responses to IRL were evaluated in the controls. There was a marked decrease in tidal volume both immediately (56 +/- 17% of baseline at an IRL of 15 cmH(2)O. l(-1). min; P < 0.001) and after 3 min of IRL (67 +/- 23%, P < 0.005). The duty cycle increased. We conclude that children with OSAS have impaired arousal responses to IRL. Despite compensatory changes in respiratory timing, normal children have a decrease in minute ventilation in response to IRL during sleep. However, arousal occurs before gas-exchange abnormalities.