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In a multicenter, double-blind, placebo-controlled rescue trial conducted at 13 Canadian hospitals, two 5 ml/kg doses of a synthetic surfactant or air placebo were administered to 344 infants with birth weights of 750 to 1249 gm who had established respiratory distress syndrome and an arterial/alveolar oxygen tension ratio less than 0.22. The first dose was given between 2 and 24 hours of age, and the second dose was given 12 hours later to the infants remaining on mechanical ventilation. Infants were stratified at study entry by birth weight and gender. The trial was terminated short of the targeted sample size because significant reductions in mortality were observed in another rescue trial completed in the United States in the same weight class of infants. Despite premature termination of the trial, the rate of survival without bronchopulmonary dysplasia was increased (61% vs 52%; p = 0.046) in infants treated with surfactant. In addition, there was a significant reduction in the incidence of overall pulmonary air leak (46% vs 32%; p = 0.009), pneumothorax (27% vs 17%; p = 0.023), and pulmonary interstitial emphysema (40% vs 28%; p = 0.018) in infants treated with synthetic surfactant. There was no difference in the incidence of bronchopulmonary dysplasia, apnea, or pulmonary hemorrhage. Significant improvements in alveolar-arterial oxygen tension gradient, arterial/alveolar oxygen tension ratio, and oxygen and ventilator requirements through day 7 were present. These findings indicate that rescue therapy with synthetic surfactant can improve outcome for premature infants weighing 750 to 1249 gm with respiratory distress syndrome.

To test the efficacy of a combined alpha- and beta-receptor agonist in acute bronchiolitis, we compared inhaled racemic epinephrine with salbutamol in a double-blind, crossover, randomized protocol. Twenty-four infants, 4.6 +/- 0.5 (mean +/- SEM) months of age, with their first episode of bronchiolitis were tested. After sedation with chloral hydrate, a clinical score and pulmonary mechanics measurements using simultaneous signals of airflow volume and transpulmonary pressure were recorded. After baseline measurements, infants received either nebulized salbutamol, 0.03 ml/kg, or racemic epinephrine, 0.1 ml/kg. Thirty minutes later, there was a significant decrease in clinical score after treatment with racemic epinephrine compared with the baseline score (p0.001); this difference was not present after salbutamol inhalation (p = 0.42). Only 13 patients had a decrease in clinical score after salbutamol therapy, in comparison with 20 infants treated with racemic epinephrine (p0.01). Both drug decreased respiratory rate, but the decrease was greater after the use of racemic epinephrine (p0.001). There was a significant decrease in inspiratory, expiratory, and total pulmonary resistance after treatment with racemic epinephrine compared with baseline values (p0.01) but no significant change after salbutamol inhalation. There was no significant correlation between the clinical score and pulmonary mechanics either at baseline or after drug treatment. We conclude that racemic epinephrine is superior to salbutamol in the treatment of infants with their first episode of acute bronchiolitis.

The effect of theophylline and cromolyn sodium on sleep was studied in 10 children with asthma who were 10 to 17 years of age (mean 13.5 +/- 2.4 years). Theophylline or cromolyn sodium was taken for 14 days in a double-blind, crossover, placebo-controlled trial. Theophylline blood levels before sleep were 10.2 +/- 4 micrograms/ml during the theophylline period. There was no difference in pulmonary function between the two periods. Theophylline did not disrupt sleep as measured by sleep latency, total sleep time, sleep efficiency, movement time, microarousals, and arousals. Apneic episodes (greater than or equal to 10 seconds) were of central origin and less frequent during the theophylline period (p less than 0.05). Arterial oxygen desaturation (greater than 5% decrease from baseline saturation when awake) was less frequent during the theophylline treatment (p less than 0.05). We conclude that theophylline treatment of the children's asthma did not disrupt sleep and appeared to have a protective effect in regard to apnea, hypopnea, and arterial oxygen saturation.

Patients with cystic fibrosis had a better acute bronchodilator response to albuterol and ipratropium bromide than to either drug alone. Further studies of long-term efficacy and safety seem justified.

We derived a noninvasive method to compare changes in cranial blood volume during mechanical ventilation with changes occurring during spontaneous breathing in newborn infants. In ten infants receiving mechanical ventilation, cranial blood volume increased during inspiration by a mean of 8.3%. We found a consistent relationship between clinical estimation of lung compliance and the amount of cranial volume expansion. During spontaneous breathing in ten infants cranial blood volume decreased during inspiration by a mean of 5.8%. The findings indicate the need for careful monitoring during periods of rapid changes in lung compliance.

To determine whether endogenous oplates play a role in the pathogenesis of perinatal asphyxia, a blinded clinical trial of naloxone, a competitive oplate receptor blocker, was undertaken in infants with low 1-minute Apgar scores. Of 85 infants with 1-minute Apgar score 0 to 3, 44 received an injection of naloxone (approximately 0.4 mg/kg) and 41 received saline solution. In 108 infants with 1-minute Apgar score 4 to 6, 54 received naloxone and 54 saline solution. In neither group was there a significant effect of naloxone on respiratory frequency or heart rate up to 30 minutes after injection, nor at 24 hours of age. In both groups active muscle tone of upper and lower limbs was increased by naloxone, a response that may not be beneficlat in the face of inadequate oxygen delivery to vital organs. We conclude that naloxone at this dose had no readily apparent benefit in the resuscitation of the asphyxiated newborn infant.

The clinical course and the results of laboratory investigations of 5 children withunilateral hyperlucent lung syndrome are presented. This syndrome appears to be an acquired disease that follows a viral bronchiolitis and pneumonitis in childhood. The adenovirus was a possible etiologic agent in 3 of the patients. The hyperlucent appearance of the lung was due to overdistention of alveoli plus a marked decrease in blood flow to the affected lung, which was smaller than normal. The ventilation of the affected side was diminished because of airway obstruction. Blood gas data obtained by selective catheterization of the pulmonary veins revealed a large intrapulmonary shunt on the affected side. Early in the course of the disease, the major branches of the pulmonary artery were not hypoplastic; it is suggested that the pulmonary artery hypoplasia, in part, results from a failure of growth on the affected side secondary to the bronchopulmonary pathology. Despite a major loss of functioning lung tissue, recurrent pulmonary infections and respiratory symptoms appeared to decrease with time.

Twenty-two premature infants, classified by breathing pattern, were studied on 47occasions with measurements of end-tidal carbon dioxide tensions and arterial P CO 2 , pH, and bicarbonate. The average arterial pH of 7.444±0.015 during periodic breathing was significantly higher than the pH of 7.396±0.012 during regular breathing (p CO 2 of the periodic group, based on end-tidal P CO 2 measurements, was estimated to be 3 or 4 mm. Hg lower than Pa CO 2 during regular breathing. The evidence suggests that there is minimal hyperventilation during periodic breathing. Premature infants breathing regularly are able to maintain a pH close to 7.40. During periodic breathing there is a cyclic change in alveolar P CO 2 of at least 6 or 7 mm. Hg. If the respiratory center responded to a change in P CO 2 as well as to the mean level of P CO 2 this could account for the slight hyperventilation. The babies appeared more wakeful during periodic breathing, could abruptly change from one breathing pattern to another, and regular breathing began at a postconceptual age of about 40 weeks. These observations suggest that the mechanism of periodic breathing may be related to a maturation phenomenon possibly associated with the central nervous system.

perplasia can be induced in an animal model? Studies on such a model might provide some illuminating differences between the diabetic State and the type of babies you have studied. DR. O m Not to my knowledge. DR. CHERNIGK, Winnipeg. Does hypoxia change the Kt value? DR. OH. I don't have any information on that. DR. R~INER, Columbus. We also see islet hyperplasia and hypertrophy in other conditions such as congenital cardiovascular disease. Have you made any observations to see if there is a correlation between the histology and the Kt ? DR. OI~. No, we haven't.

Sixty-five premature infants were examined neurologically and psychometrically duringtheir second year of life. When the neurologic status of infants who had marked tyrosinemia during their neonatal period was contrasted with that of infants whose tyrosine level remained below 15 mg. per cent, no significant difference could be detected. Although the percentage of infants with deviational I. Q. scores between 90 and 70 was significantly greater for the high tyrosine group, These differences disappeared when a deviational I. Q. score corrected for the postconceptual age was used.