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ABSTRACT: To define respiratory effects of peripheral acidemia during early development, we injected lactic acid (LA) into the jugular vein of 32 1- to 7-d-old rabbit pups and four adult rabbits. The body weight of newborns varied between 67 ± 17 g in 1-d-old and 119.8± 33.7 g in 7-d-old animals versus 4 ± 0.1 kg in adults. Animals were anesthetized with ketamine (30 mg/kg) and urethane (0.6–1.2 g/kg), tracheotomized, and breathed spontaneously. Diaphragmatic electromyogram, tidal volume, esophageal pressure, and arterial pressure were recorded. In adult rabbits, a LA dose of 0.25 mM/kg elicited an increase in the rate of breathing with no change or a decrease in tidal volume (early response), followed by a deep and fast respiration (late response). The same LA dose had no effect or provoked only the late response in 1-and 2-d-old rabbits and led to the early and late responses in older newborns. The early response was abolished and the late response was diminished after vagotomy. Our results suggest that the early response is mediated by vagal afferents and the late response, althoughmodified by vagal input, is of an extravagal origin. It is suggested that acidemia may be involved in the transient tachypnea syndrome in new born infants. Possible contribution of vagal nonmyelinated endings in triggering the early response to LA is discussed.

The potency of the Hering-Breuer inspiratory-inhibitory and expiratory-promoting reflexes decreases with maturation in mammals. The Hering-Breuer deflation reflex is present at birth and its power changes little during postnatal development. Already during the second day of life the airway defence reflex resembles that of the adult rabbits. In contrast, sensitivity of the pulmonary chemoreflex does not reach the adult level by the end of the first week of life in newborns of the same species. The time course of functional development of respiratory reflexes coincides with the maturity of different species at birth.

To define respiratory effects of peripheral acidemia during early development, we injected lactic acid (LA) into the jugular vein of 32 1− to 7-d-old rabbit pups and four adult rabbits. The body weight of newborns varied between 67 ± 17 g in 1-d-old and 119.8± 33.7 g in 7-d-old animals versus4 ± 0.1 kg in adults. Animals were anesthetized with ketamine (30 mg/kg) and urethane (0.6–1.2 g/kg), tracheotomized, and breathed spontaneously. Diaphragmatic electromyogram, tidal volume, esophageal pressure, and arterial pressure were recorded. In adult rabbits, a LA dose of 0.25 mM/kg elicited an increase in the rate of breathing with no change or a decrease in tidal volume (early response), followed by a deep and fast respiration (late response). The same LA dose had no effect or provoked only the late response in 1-and 2-d-old rabbits and led to the early and late responses in older newborns. The early response was abolished and the late response was diminished after vagotomy. Our results suggest that the early response is mediated by vagal afferents and the late response, althoughmodified by vagal input, is of an extravagal origin. It is suggested that acidemia may be involved in the transient tachypnea syndrome in new born infants. Possible contribution of vagal nonmyelinated endings in triggering the early response to LA is discussed.

Effects of 10% O2 on the response of the phrenic neurogram to vagal (VS) and saphenous stimulation (SS) were studied in anesthetized and artificially ventilated newborn (group 1: 1–3 days old, n = 13; group 2: 8–14 days old, n = 14) and adult (group 3, n = 12) rabbits. In all animals during ventilation with 100% O2 or 10% O2 in N2, VS caused a reduction in the expiratory phase (Te). Te shortening in response to SS was unaffected by hypoxia in group 3, and was abolished in group 2. In group 1 only early hypoxia blocked the Te response to SS. The preserved Te response to VS on one hand, and abolished the effects of SS on the other, suggest that blockade of the somatic inputs is due to the age-dependent action of hypoxia in areas distant to the respiratory neurons.