(1974). Archives of Disease in Childhood, 49, 796. Neonatal secretion of gastrin and glucagon. Plasma gastrin and glucagon levels were estimated in mothers after labour, and in their babies at birth and on the fourth day of life. The newly born baby appears to secrete gastrin independently and the plasma levels are higher on the fourth day of life. The cord gastrin level is lower when labour is induced or augmented by the intravenous infusion of oxytocin. Our results do not exlude the possibility that gastrin is transferred from mother to baby during a spontaneous labour. Such a maternal component of cord gastrin may be responsible for neonatal gastric hyperacidity.The mean cord glucagon level is higher than the maternal level at birth and the fourth day level is higher than the cord level. The C-terminal reactive glucagon-like inmmunoreactivity (C-GLI) in the cord blood is lower when oxytocin has been used during labour. Maternal or placental transfer of C-GLI during labour to the spontaneously born baby is one possible explanation of this finding.The raised glucagon levels on the fourth day may explain why there is low gastric acidity at this time despite the gastrin level being higher than at birth. No relation could be deduced between the C-GLI, i.e. pancreatic glucagon level, and the blood glucose level either at birth or on the fourth day of life.

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The IT method is suitable for measurement of equine TAC. TAC is lower in ponies with previous or future laminitis. The ELISA methods are not suitable for measurement of equine HMWAC or TAC.

A theory is advanced about the cause of pyloric stenosis of infancy (PS). Developmental changes will conspire to produce pathogenetic gastric hyperacidity within the first 4 weeks of life in babies who develop PS. The prime cause will be an increased gastric acidity due to a genetically determined supernormal parietal cell mass. This theory satisfactorily explains many known clinical features.

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