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11. |
Comparative Effects of Metabolic Acidemia and Hypoxemia on Cardiac Output and Regional Blood Flows in Unanesthetized Newborn Lambs |
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Pediatric Research,
Volume 20,
Issue 8,
1986,
Page 756-760
DAVID FISHER,
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摘要:
We studied the comparative effects of HC1- induced metabolic acidemia (pH=7.11 ± 0.03, mean ± SE) and hypoxemia (PO2=28 ± 1 torr) on cardiac output and regional blood flows in newborn lambs 3 days after the surgical placement of catheters in the left atrium and aorta and pacing wires on the left atrium. Cardiac output decreased by 49 ± 6% during metabolic acidemia in contrast to the 12 ± 2% increase during hypoxemia. The adrenal glands and the diaphragm were the only organs that received increased blood flows during acidemia and hypoxemia. Cerebral and myocardial blood flows decreased during acidemia but increased during hypoxemia. Blood flows decreased to the carcass and gastrointestinal tract during acidemia but did not change significantly during hypoxemia. Renal and splenic blood flows decreased during both stresses, but the reductions were more severe during acidemia. The changes in regional blood flows were not a passive result of the respective changes in cardiac output. HCl-induced metabolic acidemia and hypoxemia each result in significant redistributions of available blood flows which are quantitatively and qualitatively different from each other.
ISSN:0031-3998
出版商:OVID
年代:1986
数据来源: OVID
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12. |
Arsenate-Induced Neural Tube Defects Not Influenced by Constant Rate Administration of Folic Acid |
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Pediatric Research,
Volume 20,
Issue 8,
1986,
Page 761-762
VERGIL FERM,
DAVID HANLON,
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摘要:
Serious suggestions have been made that dietary supplementation with folic acid (FA) and perhaps other vitamins during pregnancy may reduce the incidence of neural tube defect (NTD) in human newborns. The purpose of these experiments was to evaluate the effect of continuous infusion of FA on the incidence of NTDs induced by arsenate. This teratogen induces NTDs in up to 90% of golden hamster fetuses when administered acutely during critical stages of embryogenesis. FA was administered by subcutaneously implanted osmotic minipumps beginning on the 6th day of gestation, 48 h before an acutely administered dose of sodium arsenate. The protective effect of FA was examined at three teratogenic dose levels of arsenate: optimal, with 90% NTDs, intermediate, with 38% NTDs, and low, with 20% NTDs. Fetuses were recovered at day 13 of gestation and examined for NTDs and other malformations. Maternal red cell folate levels were determined on day 8, 48 h after implantation of the pumps. The results show that the maternal red blood cell level of FA can be significantly increased within 48 h by chronic infusion to levels which are almost two times (550 ng/ml) control levels. There was no significant protection against arsenate-induced NTDs following FA supplementation at any of three levels of this teratogen.
ISSN:0031-3998
出版商:OVID
年代:1986
数据来源: OVID
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13. |
The Effects of Metabolic Acidosis on Jejunal Phosphate and Glucose Transport in Weanling Rats |
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Pediatric Research,
Volume 20,
Issue 8,
1986,
Page 763-767
STEPHEN BOROWITZ,
HAMID SAID,
FAYEZ GHISHAN,
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摘要:
To investigate the effects of metabolic acidosis on jejunal phosphate and glucose absorption,in vivoandin vitrotransport studies were performed on weanling rats fed 1.5% NH4CI for three days and on group pair-fed controls. Bothin vivoandin vitro, acidosis significantly depressed phosphate transport without effecting glucose transport.In vitro, the decrease of phosphate transport was due to a depression of sodium-phosphate cotransport, but not of sodium independent phosphate transport. This corresponded to a significant increase of the Km of sodium–phosphate cotransport with no change of the Vmax. Treatment of the acidotic animals with intraperitoneal 1,25 dihydroxycholecalciferol did not restore phosphate transport to control levels. These studies indicate that in weanling rats, metabolic acidosis selectively suppresses jejunal phosphate transport independent of circulating levels of 1,25 dihydroxycholecalciferol.
ISSN:0031-3998
出版商:OVID
年代:1986
数据来源: OVID
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14. |
An in Vitro Study of Choline Uptake by Intestine from Neonatal and Adult Rats |
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Pediatric Research,
Volume 20,
Issue 8,
1986,
Page 768-772
NANCY SHEARD,
STEVEN ZEISEL,
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摘要:
We studied choline uptake by slices of adult and 10–day–old rat intestine which were exposed on their mucosal surface to radiolabeled choline. Both neonatal and adult intestine transported choline. Choline uptake was observed in duodenum, jejunum, ileum, and colon of the adult rat. In the small intestine, choline uptake consisted of two components: a saturable and a nonsaturable process. The kinetic variables for saturable transport (Km, Vmax) were not significantly different in adult and neonatal small intestine. Some of the transported choline was converted to phosphatidylcholine, glycerophosphocholine, phosphocholine, and betaine. However, most of the transported choline (79–85%) was not metabolized within the intestinal slice during a 15-min period. We conclude that the capacity for choline transport in the rat small intestine is present early in neonatal life. The characteristics of this transport mechanism for choline are similar in the neonate and in the adult small intestine. Neonates should therefore be able to absorb the large amounts of unesterified choline that are present in milk.
ISSN:0031-3998
出版商:OVID
年代:1986
数据来源: OVID
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15. |
Infantile Sialic Acid Storage Disease: The Fate of Biosynthetically Labeled N-Acetyl-(3H)- Neuraminic Acid in Cultured Human Fibroblasts |
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Pediatric Research,
Volume 20,
Issue 8,
1986,
Page 773-777
EDUARD PASCHKE,
GERALD HOFLER,
ADELBERT ROSCHER,
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摘要:
N-acetyl-(3H)-mannosamine [(3H)-ManNAc] was used as a precursor for the metabolic labeling of Nacetyl-(3H)-neuraminic acid [(3H)-NANA] in cultured fibroblasts of a patient with infantile sialic acid storage disease (ISSD). The metabolic fate of free and bound (3H)- NANA, isolated by high-performance liquid chromatography, was followed under pulse-chase labeling conditions. Nonsaturable accumulation of free (3H)-NANA was observed in ISSD, while the metabolic flux from (3H)- ManNAc to NANA-glycoconjugates was unaffected. Accumulated free (3H)-NANA could not effectively be chased from ISSD cells although N-acetyl-(3H)-hexosamines [(3H)-HexNAc] were appearing in the chase medium. These metabolites could arise from (3H)-NANA bound to glycoconjugates which were cleaved at normal rates in ISSD. The finding that free (3H)-NANA was markedly increased relative to its major products (3H)-HexNAc is suggestive for an impaired degradation and reutilization of (3H)-NANA due to trapping in a metabolically unaccessible pool. In titration experiments with digitonin a clear-cut increase in the latency of labeled NANA relative to a cytoplasmic marker enzyme was evident in ISSD. The release of (3H)-NANA, however, followed closely the digitonin- induced release of the lysosomal enzyme β-hexosaminidase. This is suggestive for a lysosomal location of the stored material.
ISSN:0031-3998
出版商:OVID
年代:1986
数据来源: OVID
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16. |
Cerebral Blood Flow and O2 Metabolism after Asphyxia in Neonatal Lambs |
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Pediatric Research,
Volume 20,
Issue 8,
1986,
Page 778-782
ADAM ROSENBERG,
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摘要:
A neonatal lamb model has been developed to examine the regulation of cerebral blood flow (CBF) and oxygen metabolism during the critical period after an asphyxial insult. Nine newborn lambs had control measurements and timed measurements after asphyxia of CBF (radioactive microsphere technique), arterial and cerebral venous (sagittal sinus) blood gases and oxygen contents performed. Immediately after resuscitation from asphyxia, there was a marked increase in CBF compared to control (239 ± 22 versus 82 ± 7 ml 100 g-1min-1, mean ± SEM; p<0.01). Cerebral oxygen delivery (CBF x arterial O2content) increased from 12.87 ± 1.20 to 37.40 ± 3.40 ml- 100 g-1.min-1(p<0.01), while cerebral O2consumption was significantly decreased compared to control (4.75 ± 0.42 to 3.42 ± 0.46 ml 100 g-1. min-1, p<0.05). Cerebral fractional O2extraction, the relationship between oxygen uptake and delivery fell from 0.38 ± 0.03 to 0.09 ± 0.02; p<0.01. This reactive hyperemia was followed in all animals by a period of hypoperfusion. CBF (52 ± 4 ml .100 g-1min-1), O2delivery (7.94 ± 0.50 ml 100 g-1- min-1), and cerebral O2consumption (3.34 ± 0.24 ml-100 g-1. min-1) were all significantly depressed when compared to control. These data demonstrate important changes in CBF and O2metabolism after neonatal asphyxia that may be important to the pathogenesis of brain injury.
ISSN:0031-3998
出版商:OVID
年代:1986
数据来源: OVID
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17. |
Pancytopenia in Propionic Acidemia: Hematologic Evaluation and Studies of Hematopoiesis in Vitro |
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Pediatric Research,
Volume 20,
Issue 8,
1986,
Page 783-788
LINDA STORK,
DANIEL AMBRUSO,
STEPHEN WALLNER,
JAMES SAMBRANO,
LYNN MOSCINSKI,
HARRY WILSON,
EDWARD McCABE,
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摘要:
This study investigated the hematologic abnormalities of an infant with propionic acidemia and reversible pancytopenia. Light and electron microscopy of her bone marrow revealed severely disturbed cellular morphology with trilineage dysmyelopoiesis, hemophagocytosis, and numerous multinucleated histiocytes and megakaryocytes. The effects of her serum and of organic acids associated with propionic acidemia were studied on hematopoiesis in vitro. Mouse erythroid (CFU-E) and granulocyte- monocyte colonies (CFU-GM) were assayed by fibrin clot technique; human CFU-GM were grown in agar culture. The infant's serum reduced mouse CFU-E and CFUGM by 43 and 32%, respectively, compared with normal human sera, but had no effect on human CFU-GM in our culture system. Buffered propionic acid caused concentration- dependent inhibition of mouse CFU-E and human CFU-GM over a range reported in sera of acutely ill infants with propionic acidemia. Neither cell viability nor subsequent colony formation was diminished by preincubation of bone marrow cells with propionic acid for 48 h. The three other organic acids studied, tiglic acid, 3-OH propionate, and glycine, did not inhibit growth of mouse CFUE, CFU-GM, or human CFU-GM, and glycine significantly enhanced formation of the latter. Evaluation of the infant's hematologic abnormalities suggests that inhibition of bone marrow proliferation and maturation and, perhaps, shortened red blood cell survival were responsible for her pancytopenia. The studies performed in vitro implicate propionic acid in this hematopoietic dysfunction.
ISSN:0031-3998
出版商:OVID
年代:1986
数据来源: OVID
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18. |
Experimental Bilirubin Encephalopathy: Importance of Total Bilirubin, Protein Binding, and Blood-Brain Barrier |
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Pediatric Research,
Volume 20,
Issue 8,
1986,
Page 789-792
RICHARD WENNBERG,
A J HANCE,
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摘要:
The cause of bilirubin encephalopathy has been variously ascribed to elevated total serum bilirubin concentration, high free bilirubin levels (or impaired albumin binding), and disruption of the blood-brain barrier. An experimental rat model for acute bilirubin encephalopathy was developed in which these three factors could be varied independently. Osmotic opening of the blood-brain barrier in the right hemisphere was produced by infusing a hypertonic arabinose solution into the right carotid artery. The total bilirubin level and bilirubin binding state were varied by adjusting the amount of bilirubin infused intravenously and/or by infusing human serum albumin. Brain electrical activity (EEG) served as an indicator of developing encephalopathy. Neither staining nor EEG changes occurred if the blood-brain barrier remained intact. Bilirubin staining without EEG evidence of encephalopathy sometimes occurred when the blood-brain barrier was open. Discriminant analysis showed that EEG changes were best predicted by the degree of blood-brain barrier opening (as indicated by brain bilirubin content) and by the quality of serum bilirubin binding. Serum total bilirubin concentration was not an important discriminator of encephalopathy.
ISSN:0031-3998
出版商:OVID
年代:1986
数据来源: OVID
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19. |
Effect of Nutritional Rehabilitation on the Development of Intestinal Brush Border Disaccharidases of Postnatally Malnourished Weanling Rats |
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Pediatric Research,
Volume 20,
Issue 8,
1986,
Page 793-797
THOMAS ROSSI,
P C LEE,
CAROLYN YOUNG,
AARON LERNER,
EMANUEL LEBENTHAL,
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摘要:
The reversibility of the effects of postnatal malnutrition on the intestinal brush border enzymes and somatic and intestinal weights were examined using either ad libitum or restricted feedings. Malnutrition was induced in the immediate postnatal period by expanding newborn rat litters to 20 pups/dam. At 21 days of age, malnourished pups exhibited significantly decreased body and intestinal weights as compared to those from control litters. Malnourished pups also had significantly elevated lactase specific activities whereas sucrase and maltase activities were not affected in the proximal small intestine. With subsequent nutritional rehabilitation by an ad libitum (food available 24 h/day) or restricted feeding regimen (food available 2 h/day), body and intestinal weights remained significantly depressed by 56 days in malnourished as compared to control animals. Rats on 2–h feedings consumed approximately 35% of the food consumed by their ad libitum-fed counterparts. Comparison of the ratio of weight gained to the amount of food consumed did not demonstrate a greater food efficiency with any particular feeding pattern. With ad libitum or restricted feedings, lactase specific activity in the proximal segment attained control values by 14 days. Restricted feedings resulted in an apparent elevation of specific activity of sucrase and of maltase, when rats were sacrificed at one chosen time point. Multiple time studies in a 24–h cycle showed that maximal elevations in enzyme activities were associated with feeding time. There were no significant differences in mean specific daily enzyme activities between the two feeding regimens. Restricted feedings show no advantage in enzyme efficiency or in promoting the rate of recovery of the intestine after postnatal malnutrition.
ISSN:0031-3998
出版商:OVID
年代:1986
数据来源: OVID
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20. |
Effect of Hypercapnic Acidosis on Renal Function in the Newborn Rabbit |
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Pediatric Research,
Volume 20,
Issue 8,
1986,
Page 798-801
A J V D HEIJDEN,
J P GUIGNARD,
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摘要:
Anaesthetized mechanically ventilated newborn rabbits were exposed to different degrees of hypercapnia. One hour of normocapnia was used as a control period. Renal function studies demonstrated an increase in renal vascular resistance with a concomitant decrease in effective renal plasma flow in all hypercapnic animals, combined with a less pronounced decrease in glomerular filtration rate. Filtration fraction rose significantly. A decrease in systemic blood pressure was only observed when the PaCO2exceeded 100 mm Hg combined with an arterial pH below or equal to 7.10. We conclude that normoxemic hypercapnia in the newborn rabbit leads to an increase in renal vascular resistance and suggest that the renal vasoconstriction predominates at the level of the efferent arteriole.
ISSN:0031-3998
出版商:OVID
年代:1986
数据来源: OVID
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