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Oxidative decarboxylation of pyruvate by branched-chain 2-oxo acid dehydrogenase can result in overestimation of the expressed and total activity of hepatic pyruvate dehydrogenase. Pyruvate is a poor substrate for branched-chain 2-oxo acid dehydrogenase relative to the branched-chain oxo acids; however, the comparable total activities of the two complexes in liver, the much greater activity state of branched-chain 2-oxo acid dehydrogenase compared with pyruvate dehydrogenase in most physiological states, and the use of high pyruvate concentrations, explain the interference that can occur in conventional radiochemical or indicator-enzyme linked assays of pyruvate dehydrogenase. Goat antibody that specifically inhibited branched-chain 2-oxo acid dehydrogenase was used in this study to provide a more specific assay for pyruvate dehydrogenase.

Hyaline membranes in 21 of postmature infant autopsies were studied, using 27 term infant autopsies as the control population. The occurrence of hyaline membranes was much higher in postterm (86%) than term infant autopsies (26%). Seventeen of 21 postmature infants had clinical and microscopic evidence of aspiration, contaminated by meconium in 14, suggesting that meconium and/or amniotic aspiration may be an etiologic factor in postmature hyaline membrane formation. Thirteen infants had severe hyaline membrane formation, microscopically distinguishable from hyaline membrane disease of the premature only by the maturity of the underlying lung. Besides the pulmonary findings, little difference in organ histology was observed between the two groups. This study showed that hyaline membrane formation resulted in asphyxia and respiratory failure in the majority of the postmature infants who were already troubled with hypoxia and a combined respiratory and metabolic acidosis secondary to meconium aspiration, and eventually led to death.