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sodium cromoglycate. This effect was not due to a difference between the patients, since when we recalculated the results using the same 11 subjects for both placebo and sodium cromoglycate they were the same. Sodium cromoglycate has a slight phosphodiesterase inhibiting effect, which might explain the differences' 0; however, it has no effect on the histamine response of human bronchial smooth muscle.' We have also shown that sodium cromoglycate has no effect on tracheal smooth-muscle contraction induced by histamine or methacholine."1 It does, however, inhibit allergen contraction of the passively sensitised human tracheal smooth muscles.Our results of the lack of effect of sodium cromoglycate on histamine challenge are consistent with those of Pagelow.'2 He found no difference in the threshold of histamine bronchial reactivity with sodium cromoglycate or phentolamine. In contrast, Kerr et alt7 reported complete protection against histamine with both these agents. We have studied the effect of sodium cromoglycate in vitro on the alpha-receptor contraction of isolated human trachea induced by adrenaline in the presence of propranolol. In this system we are unable to show any inhibition by sodium cromoglycate of alpha-receptor contraction.13

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The cause of fetal distress and neonatal respiratory distress (RD) in association with meconium-stained liquor is not always clear. To clarify this, a prospective study was undertaken in a tertiary referral maternity hospital for 1 year. In all infants born after meconium-stained liquor who developed RD, evidence was sought for 1) fetal distress (from the cardiotocograph (CTG), the cord blood pH, the Apgar score and the asphyxial complications in the neonate) 2) causes of fetal distress (including maternal risk factors, fetal infection and fetal malnutrition) 3) causes of respiratory distress (including meconium aspiration syndrome (MAS), persistent pulmonary hypertension of the newborn (PPHN) and infection). Of 4,026 livebirths, 717 (17.8%) had meconium-stained liquor and 44 term and 5 preterm infants developed RD. In the 44 term infants, there was frequent evidence of fetal distress possibly caused by previously unrecognized factors such as fetal malnutrition with reduced neonatal skinfold thickness in 35% triceps and 41% subscapular measurements, and histological chorioamnionitis (CA) in 74%. The cause for respiratory distress was identified in only 48% of infants, and included clinical evidence of PPHN (41%), MAS (16%) and infection (2%). However in preterm infants, 80% had definite or suspected infection. The findings indicate that fetal distress is common in infants who develop respiratory distress after meconium-stained liquor. A role for histological CA and reduced nutrition in the fetus, as factors contributing to the vulnerability of the term infant to intrapartum fetal distress, is suggested.

SYNOPSIS Pharyngeal incoodination is an occasional cause of regurgitation and respiratory distress in the neonate, but it can cause an aspiration pneumonia which may be lethal. Usually the condition is self‐limited and followed by recovery in 1 or 2 weeks. We report a case in which the manifestations, including recurrent attacks of bronchopneumonia, lasted for 3 years and were eventually followed by normal function.