Panel report on nutritional support of pediatric patients.
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Biomedical subjects
Publications and source records attributed to W C Heird.
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In beagle pups (from 5 to 84 days of age), plasma taurine concentration decreased between 5 and 21 days of age with no change thereafer; cerebral taurine concentration decreased throughout the period of study but cerebral taurine content increased between 5 and 21 days of age; hepatic taurine content (but not concentration) increased throughout. Both hepatic cysteinesulfinic acid decarboxylase (CSAD) activity and the concentration of taurine-conjugated bile acid of gallbladder bile increased during the period of study. Plasma and cerebral taurine pools were not affected by taurine-free total parenteral nutrition (TPN). Hepatic taurine content was also not affected, but taurine concentration decreased; however, this change resulted from an increase in hepatic size. Hepatic CSAD activity of animals that received TPN was greater than that of 35-day control animals while the concentration of taurine-conjugated bile acids in the gallbladder bile was less. Although plasma taurine concentration was not affected by intravenous glucose therapy, both the hepatic taurine concentration and content of these animals were less than those of 35-day control animals. Cerebral taurine concentration of these animals, on the other hand, were greater. Hepatic CSAD activity of the animals that received only intravenous glucose was similar to that of controls, but the taurine-conjugated bile acid concentration in the gallbladder bile, like that of animals that received TPN, was less than that observed in 35-day control animals.
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Various membrane transport functions have been studied in erythrocytes from essential fatty acid (EFA) deficient rats in order to determine whether or not functional abnormalities induced by documented EFA-deficiency of the membrane could be demonstrated. No differences were found between EFA deficient and control cells with respect to mean values for osmotic resistance or intracellular sodium and potassium concentrations. However, uptake of leucine by EFA deficient erythrocytes was significantly greater than that of control erythrocytes. Kinetic studies suggest that EFA deficiency enhances the passive diffusion component of this transport.
A controlled study comparing two intravenous fluid regimens was performed in sick, premature infants. The regimens were isocaloric at 60 calories/kg/day, one providing glucose alone, the other glucose plus 2.5 gm/kg of amino acids. There was no difference in changes in body weight between the two groups; infants receiving glucose alone were in negative nitrogen balance; those receiving glucose plus amino acids were in positive nitrogen balance. Plasma amino acid values were compared to published, postprandial normal values. The TEAA and TAA of infants receiving amino acids were not different from normal. Values of TEAA and TAA of infants receiving glucose alone were significantly lower. Essential fatty acid deficiency developed in infants receiving amino acids but not in those receiving glucose alone. It is concluded that the glucose plus amino acid regimen results in anabolism without undue metabolic costs.
Adenine nucleotide content and adenine nucleotide transport were evaluated in rats deficient in essential fatty acids (EFA) and in control rats. ADP uptake by EFA-deficient mitochondria was altered in a manner similar to the alteration produced by treatment of normal mitochondria with uncoupler. The uptake of ATP by EFA-deficient mitochondria was more rapid than that of normal mitochondria, but similar to that of normal mitochondria treated with uncoupler (DNP). Both uptake of ADP and uptake of ATP by EFA-deficient mitochondria were atractyloside sensitive. Total adenine nucleotide content of liver mitochondria from EFA-deficient rats was similar to that of liver mitochondria from control animals, but the content of ATP in EFA-deficient mitochondria was significantly higher than that of normal mitochondria. There was a negative correlation between the concentration of linoleic acid in total mitochondria lipids and ATP content of mitochondria.
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A rat model of necrotizing enterocolitis of the neonate in which maternal milk had been protective was studied to determine what components of the milk afforded protection and by what mechanism. Frozen and thrawed rat milk was not protective, but formula supplemented with rat milk cells was. It was concluded that the cells provided protection. The cells, which are principally mononuclear phagocytes, can phagocytize and kill the Klebsiella pneumoniae strain used in the animal model. Animals with necrotizing enterolitis had peritonitis and bacteremia caused by this bacillus.
The effects on hepatic growth of fat-free TPN and semistarvation have been studied in newborn beagle puppies. Our data indicate that liver growth during TPN is characterized by normal deposition of protein and minerals, with increased glycogen and decreased lipid content. While the lipid pattern of TPN livers is normal, the phospholipid fraction contains an abnormal fatty acid pattern, consistent with the development of essential fatty acid deficiency. The exact physiologic significance of this is unknown, but it is tempting to speculate that changes in integrity of the hepatic cell membrane as a result of this abnormal fatty acid pattern might account for some of the clinical abnormalities of hepatic function during TPN.
Despite the fact that necrotizing enterocolitis is considered a disease of premature infants, 20% of all affected infants at Babies Hospital over the past 20 years were products of term gestations. Two distinct subgroups of such infants were noted (1) five infants with congenital heart disease and/or congestive heart failure (e.g.hypoplastic left heart syndrome), all but one of whom developed the disease in the first week of life; (2) eight infants who developed the disease at a much later age after a protracted period of diarrhea. This histopathologic features of the disease in term infants are the same as those in premature infants. Further, the pathogenesis of the disease in term infants does not appear to differ basically from that in premature infants. These facts, lead away from the concept of NEC as a disease of simple etiology.
The intriguing observation that cutaneous application of essential fatty acid (EFA)-rich oil corrects the biochemical abnormalities of EFA deficiency was evaluated in EFA-deficient rats. Approximately 185 mg of safflower oil (140 mg of linoleic acid) were applied daily for 15 days to the kin of EFA-deficient rats. Before and after treatment with the safflower oil, the fatty acid patterns of plasma and erythrocyte phospholipid as well as of plasma triglyceride and cholesterol ester fractions were determined. The linoleic and arachidonic acid content of both plasma and erythrocyte phospholipid increased, while the eicosatrienoic acid content of both fractions decreased. The linoleic acid content of plasma triglyceride increased with safflower oil treatment, but little change occurred in the almost undetectable pretreatment levels of arachidonic and eicosatrienoic acid. In the plasma cholesterol ester fraction, arachidonic acid increased with treatment and eicosatrienoic acid decreased, but the small increase in the linoleic acid content was not statistically significant. Thus, the study confirms the observation that cutaneous application of EFA-rich oils reverses the plasma biochemical manifestation of EFA deficiency. In addition cutaneously applied EFA-rich oils reversed the biochemical manifestations of EFA deficiency in erythrocytes. Whether or not cutaneous application of such oils will prevent EFA deficiency, however, remains to be proven.
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Sixty-four cases of necrotizing enterocolitis are reviewed. The diagnosis was based on tissue examination in 57 and on the clinical syndrome, including pneumatosis, in 7. Three factors are important in the development of the disease: injury to the intestinal mucosa, bacteria, and feedings. The indications for surgical intervention are pneumoperitoneum, signs of peritonitis, and intestinal obstruction. The importance of stress in the etiology of the disease is confirmed by the high incidence of perinatal complications, particularly hypoxia. The mortality was high, but results are improving with the institution of early aggressive treatment.