Minimal Rates of Oxygen Consumption in Sick and Premature Newborn Infants

Abstract

The total energy expenditure of the living organism has been the subject of interest and research since the eighteenth century when Lavoisier made the fundamental observation that energy is produced in the body by the process of oxidation. Kern, 1928;Bruin, 1931)). Some authors, Received January 31, 1966. therefore, prefer the term 'standard metabolism' (Bierring, 1931;Du Bois, 1936;Karlberg, 1952).With a baby, the fasting state is unsatisfactory for examining 'basal' metabolism. He is always digesting one meal or actively anticipating the next. Lee and Iliff (1956) showed in older babies and children that metabolic rate in the awake and fasting state is higher than when the child is in post-prandial sleep. Some workers have chosen the fasting state using a small dose of barbiturate to prevent 'uneasiness' (Baer, 1929;Schadow, 1929;Karlberg, 1952). The 'specific dynamic action' of food in infants is less pronounced than in adults, the maximal increase in energy metabolism being of the order of 4-10% after an ordinary feed (McCance and Strangeways, 1954;Levine, Wilson, and Gottschall, 1928).Until about 1940, the importance of environmental temperature and neutral range in babies was not fully appreciated. In 1943 Day, Curtis, and Kelly showed that premature babies more than a week old increased metabolism in the cold, but as recently as 1958 Silverman, Fertig, and Berger were unable to find satisfactory evidence that premature babies less than a week old had a metabolic increase in the cold. The result is that, in much of the early work, it is far from clear whether babies were in a neutral thermal environment when 'basal metabolism' was measured. To avoid assumptions implicit in terms 'basal' or

Oxygen consumption in normally grown, small‐for‐dates and large‐for‐dates new‐born infants

“…Values for the small-for-dates babies run consistently about 10 % higher than those of full-terms, but this is probably merely a reflexion of the fact small-for-date babies are light in weight largely because they possess a smaller amount of subcutaneous fat (which has a low metabolic rate compared with the rest of the body as a whole) than do other full-term babies. Sinclair & Silverman (1966) and Scopes & Ahmed (1966) both reported a somewhat higher V02/kg in small-for-dates babies than in babies whose weight was within normal limits for gestational age.…”

Longitudinal Studies on Metabolic Rate, Heat Loss, and Energy Cost of Growth in Low Birth Weight Infants

“…The metabolic rate of LBW infants at rest has been calculated in many studies of oxygen consumption. Many authors (3,7,9,12,16,17,23,25,28) have shown that it increases slowly during the first week. It is not known if the oxygen consumption at rest increases after the age of 1 wk.…”

Intrauterine Growth-Retarded Rat Pups Show Increased Susceptibility to Pulmonary O2 Toxicity

“…The cyanotic appearance, gasping respirations, and nasal frothing of the pups just prior to their deaths, together with the grossly swollen appearance of the lungs clearly indicated to us a pulmonary cause for their demise. In examining the literature for other parameters that are different in normally nourished and growthretarded newborns we have found the following data which could partially explain the accelerated pulmonary O2 toxicity in the IGR pups: (1) small for gestational age newborns are reportedly in a relatively hypermetabolic state with increased rates of O2 consumption-experimentally produced hypermetabolism with increased O2 consumption results in greater 0,-free radical production and an acceleration of 0 2 toxicity (30,32,34,35); (2) IGR rat pups reportedly have depressed capacity for ATP synthesis (36), and depressed capacity for DNA synthesis and cell proliferation (37, 38)-both of these characteristics could be important in depressing the repair response to ongoing 02-induced lung cell injury; and finally, (3) purely postnatal adaptations in other organs (brain myelination) have been found to be altered by malnutrition during the prenatal period only (39). Further studies will obviously need to be done to understand why prenatal malnutrition appears to have as marked a detrimental effect on tolerance/susceptibility to pulmonary O2 toxicity as postnatal nutritional deficiency is now known to have.…”