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Abstract, It has been suggested that apnea of prematurity may be caused by "immaturity" of central control of breathing. To test the validity of this hypothesis tidal volume (V[sub T]), alveolar ventilation (V[sub A]), alveolar PCO[sub 2] (P[sub A]CO[sub 2]), esophageal pressure change, and the slope of the CO[sub 2] response curve (change AV[sub E] [minute ventilation]/change P[sub A]CO[sub 2]) were determined in 18 infants with apnea (mean of 32 episodes of more than 20 seconds duration per day) and in 18 healthy newborns used as control subjects. The infants were matched for birth weight (1,068 g v 1,065 g), gestational age (30.2 weeks v 30.2 weeks), and postnatal age (8.6 days v 8.3 days). The results were as follows: V[sub T] (4.4 +/- 1.0 mL/kg v 5.3 +/- 1.6 mL/kg), V[sub A] (96 +/- 21 mL/ kg/min v 129 +/- 33 mL/kg/min), P[sub A]CO[sub 2] (45.4 +/- 8.5 mm Hg v 35.6 +/- 4.7 mm Hg), esophageal pressure change (4.5 +/- 0.9 cm H[sub 2]O v 6.0 +/- 1.8 cm H[sub 2]O), change V[sub E]/change P[sub A]CO[sub 2](20.2 +/10.6 mL/min/kg/mm Hg CO[sub 2] v 40.7 +/-19.9 mL/min/kg/ mm Hg CO[sub 2]). There was a significant difference between infants with and without apnea for all measurements. The results indicate a decreased respiratory center output and a depressed ventilatoty response to CO[sub 2] in infants with apnea. As there was no difference between the two groups in pulmonary mechanics or oxygenation, the findings support the hypothesis that a central disturbance in regulation of breathing is the cause of apnea in these infants. [ABSTRACT FROM AUTHOR]

Abstract. Airway obstruction is a cause of apnea in preterm infants. The activity of protective respiratory reflexes was determined in 18 preterm infants with apnea (mean of 32 episodes of more than 20 seconds duration per day) and in 18 neonates without apnea used as control subjects. This was done in order to elucidate the role of respiratory reflexes in apnea of prematurity. The infants were matched for birth weight (1,068 g v 1,065 g), gestational age (30.2 weeks v 30.2 weeks), and postnatal age (8.6 days v 8.3 days). The airway occlusion technique was used to determine the inspiratory prolongation of the occluded breath and the effective elastance of the respiratory system. Inspiratory prolongation is a measure for the reflex influence on inspiratory duration, and effective elastance reflects load compensating ability. Inspiratory prolongation was 7.3% +/- 33.5% in infants with apnea and 30.6% +/- 22.7% in the control group (P < .025). Effective elastance was 1.1 +/- 0.5 cm H[sub 2]O/mL in the apneic group and 1.5 +/- 0.5 cm H[sub 2]O/mL in the infants without apnea (P < .025). The results indicate that during exposure to respiratory loads, the infants with apnea maintained inspiratory effort poorly and had a decreased ability for load compensation. Their respiratory reflexes were significantly more immature than the reflex activity of the infants without apnea. This functional immaturity of respiratory reflexes may be a contributing factor in the etiology of apnea of prematurity. [ABSTRACT FROM AUTHOR]

ABSTRACT. The effects of aminophylline on the respiratory center output were studied in 14 premature infants with idiopathic apnea. The mean birth weight was 1,052 gm, and the mean gestational age was 30.2 weeks. These infants had a normal expired volume per minute (VE) [291 ml/(min x kg)] and a normal esophageal pressure change per breath (4.5 cm H[sub 2]O); however, their alveolar ventilation per minute (VA) was decreased [89 ml/(min x kg)], resulting in an elevated end-tidal PCO[sub 2] (P[sub A]CO[sub 2]) [47.8 mm Hg]. The reasons for the elevated P[sub A]CO[sub 2] were the relatively large anatomical dead spaces (VD) found in these infants (3.4 ml/kg), and a decreased slope of the CO[sub 2] response curve [22.2 ml/ (min x kg x mm Hg P[sub A]CO[sub 2])], with a shift of the curve to the right. Oxygen consumption was normal [7.0 ml/(min x kg)]. Forty-eight hours after initiating treatment with aminophylline (2 mg/kg of body weight every six hours), the incidence of apneic episodes decreased from 29.7 to 4.4 per 24 hours, VA and P[sub A]CO[sub 2] became normal secondary to a 33% increase in esophageal pressure change per breath, and the position of the CO[sub 2] response curve showed a significant shift to the left without change in slope. Oxygen consumption increased 20% from basal value. These findings support the hypothesis that apnea in premature infants is related to an immature respiratory center characterized by a decreased output. Aminophylline probably increases respiratory center output by lowering the threshold of the central chemorecepter to CO[sub 2]. [ABSTRACT FROM AUTHOR]