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11. |
Inhibition of Na+Reabsorption in the Rat Parotid Gland by Prostaglandin E1and KallidinImplications for Cystic Fibrosis |
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Pediatric Research,
Volume 15,
Issue 11,
1981,
Page 1439-1442
J. MARTINEZ,
JEAN CAMDEN,
FRANCES BONEY,
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摘要:
SummaryProstaglandin E1caused a dose-related inhibition of sodium reabsorption in the rat parotid gland when injected by retrograde perfusion into the glandular ducts. The extent of inhibition ranged from 11.7 ± 2.4% at a dose of 2.5 μg to 63.8 ± 8.9% at a dose of 31.2 μg. Both phospholipase A2, an enzyme involved in prostaglandin synthesis, and arachidonic acid, a precursor of prostaglandins, also increased the Na+concentration of parotid saliva in a dose-dependent fashion. With phospholipase A2the inhibition ranged from 21.6 ± 4.4% at a dose of 3 μg to 73.5 ± 8.2% at a dose of 30 μg. With arachidonic acid, the degree of inhibition was 5.1 ± 3.0% at a 10-5M dose and 57.7 ± 10.2% at a dose of 10-3M. Lysine bradykinin (kallidin), a peptide present in salivary and other exocrine glands and their secretions, also caused a 30% inhibition of Na+reabsorption when retroperfused at a concentration of 12.5 μg, as did kallikrein (176 μg) and trypsin (33.3 μg). These results indicate that prostaglandins and kinins can inhibit Na+reabsorption in the rat parotid duct when present in the luminal side of the cells. Since they are normally present in exocrine glands and can presumably be secreted, they may have a role as luminal factors in the regulation of transductal transport of Na+. The possibility that they may be increased in the exocrine secretions of patients with cystic fibrosis and that they may act as the so-called cystic fibrosis “factors” is also raised by the findings of this study.
ISSN:0031-3998
出版商:OVID
年代:1981
数据来源: OVID
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12. |
Glucose‐6-Phosphate Dehydrogenase Red Blood Cell Phenotype in GdMediterraneanHeterozygous Females and Hemizygous Males at Birth |
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Pediatric Research,
Volume 15,
Issue 11,
1981,
Page 1443-1446
G. SANNA,
F. FRAU,
S. VIRGILIIS,
P. PIU,
F. BERTOLINO,
A. CAO,
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摘要:
SummaryThe distribution of red blood cell G6PD phenotype was studied by means of the methemoglobin elution test in newborn (46) and adult (50) GdMediterraneanheterozygous females and newborn (20) and adult (30) hemizygous males. Newborn heterozygotes had a statistically significant (P< 0.0005) lower mean red blood cell G6PD enzymatic activity (3.23 ± 1.04) than did normal newborns (8.78 ± 1.91), whereas there was no significant difference (P> 0.30) from the mean of adult heterozygotes (2.93 ± 0.86). Like adults, newborn heterozygous females showed: (1) a clear correlation (P< 0.001) between the percentage of enzyme-deficient red blood cells and G6PD enzymatic activity; and (2) the expected two red blood cell population,i.e., one deficient and the other normal (mosaicism). However, in newborns, the distribution of the subjects according to G6PD-deficient red blood cell percentage (mean percent, 43.67) was significantly shifted (P< 0.025) in favour of the normal phenotype, unlike adult heterozygotes, who showed a symmetrical distribution of G6PD positive and negative red blood cells (mean percent G6PD-deficient red blood cells, 53.27;P> 0.20). Newborn hemizygous males showed a consistent percentage (average, 8.28 ± 2.2) of stained red blood cells due to the presence of young erythrocytes (pseudomosaicism) unlike the occasional stained cells (≤5) seen in adults. The prevalence of hyperbilirubinemia in hemizygous males and heterozygous females was 10.22 and 2.2%, respectively, whereas in G6PD normal newborns it was 5.1%. The practical implication of this study is that the diagnosis at birth of the heterozygous state for G6PD deficiency of the Mediterranean type may be more difficult than in adults. Therefore, very sensitive methods, such as the methemoglobin elution test, should be carried out.
ISSN:0031-3998
出版商:OVID
年代:1981
数据来源: OVID
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13. |
Renal Pathogenesis of Familial HyperuricemiaStudies in Two Kindreds |
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Pediatric Research,
Volume 15,
Issue 11,
1981,
Page 1447-1453
F. STAPLETON,
WILLIAM NYHAN,
MARGARET BORDEN,
I. KAUFMAN,
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摘要:
SummaryThe pathogenesis of familial hyperuricemia has been investigated in two kindreds in whom hyperuricemia was present in members of successive generations. Enzymatic and metabolic studies, including the incorporation of isotopically labeled glycine into urinary uric acid and assessment of the total excretion of oxypurines in one family, excluded a metabolic etiology. No secondary cause of hyperuricemia was identified in either family. Fractional excretion of uric acid was less than 6.2% in all hyperuricemic individuals studied, while creatinine clearances were normal. Tubular secretion of uric acid and tubular reabsorption of uric acid were studied in an affected teenager from each family while receiving a purine-free diet. Inhibition of secretion of uric acid with pyrazinamide decreased fractional excretion of uric acid to 0.6% in patient S and to 0.7% in patient B. Tubular secretion of uric acid at maximal response to pyrazinamide in these patients was 0.393 and 0.410 mg/dl glomerular filtration rate (nl response 0.300 to 1.30 mg/min/100 ml inulin clearance). Probenecid, an inhibitor of uric acid reabsorption, increased uric acid excretion by 3.9 rag/min and by 3.2 mg/min (nl response 1.7 ± 03 mg/min) in patients S and B. Tubular reabsorption of uric acid distal to secretory sites was determined by assessing the uricosuric response to probenecid plus pyrazinamide. Uric acid excretion increased by only 0.08 mg/min in patient A and by 0.17 mg/min in patient B (nl response 0.9 mg/min). Ascorbic acid increased fractional excretion of uric acid by 7.2% in patient S but was not uricosuric in patient B or any hyperuricemic member of his family. These data suggest that hyperuricemia in these families is due to diminished renal clearance of uric acid and that the reduced clearance is due to increased tubular reabsorption of uric acid distal to secretory sites.
ISSN:0031-3998
出版商:OVID
年代:1981
数据来源: OVID
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14. |
Nitrogen Metabolism in Preterm Infants Fed Human Donor Breast Milkthe Possible Essentiality of Glycine |
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Pediatric Research,
Volume 15,
Issue 11,
1981,
Page 1454-1461
A. JACKSON,
J. SHAW,
A. BARBER,
M. GOLDEN,
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摘要:
SummaryNitrogen metabolism was studied in three preterm infants (mean gestation 32 wk) by the method of consecutive metabolic balance. The absorption and retention of nitrogen from breast milk was measured, and protein turnover, synthesis, and breakdown were calculated from isotopic plateau of urinary urea and ammonia using an intermittent oral administration of15N-glycine. Weight gain and nitrogen retention were compared with the weight gain and nitrogen accumulated for a foetus of equivalent gestational agein utero.The average composition of the milk was 289 ± 19 KJ dl-1and 1.44 ± 24 g protein dl-1. The intake of energy was 572 ± 61 KJ kg-1day-1and of nitrogen 447 ± 99 mg kg-1day-1. Stool output of nitrogen was 100 ± 32 mg kg-1day-1giving an absorption of 348 ± 78 mg kg-1day-1, as urinary excretion was 91 ± 17 mg kg-1day-1retained nitrogen was 256 ± 71 mg kg-1day-1, or 56% of intake.The specific weight gain was 15.6 ± 2.6 g kg-1day-1and 53% of this comprised lean tissue (range 34 to 89%). In all but one study the postnatal retention of nitrogen fell far short of calculatedin uteroaccumulation.The results of protein turnover were surprising. In six of the eight studies urinary urea failed to become enriched at all. Protein turnover calculated from the ammonia plateau was 1.94 ± 0.54 g nitrogen kg-1day-1, synthesis 10.9 ± 3.4 g protein kg-1day-1and breakdown 9.3 ± 3.4 g protein kg-1day-1.It is concluded that the amino acid composition of breast milk may be inappropriate for supporting rates of lean tissue deposition equivalent toin uteroaccumulation.
ISSN:0031-3998
出版商:OVID
年代:1981
数据来源: OVID
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15. |
ABNORMAL HYPERCARBIC AND HYPOXIC SLEEP AROUSAL RESPONSES IN NEAR‐MISS SIDS INFANTS |
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Pediatric Research,
Volume 15,
Issue 11,
1981,
Page 1462-1464
Carl Hunt,
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摘要:
SummaryArousal responses (AR) to hypercarbia and to hypoxia were ascertained in 25 N-M SIDS infants and 21 control infants in whom ventilatory responses to hypercarbia and hypoxia were also measured. Although the frequency of a positive AR to hypercarbia was not significantly less in the N-M SIDS compared to control group, the overall pattern was a generally absent AR in the lowest hypercarbic ventilatory response slope group progressing to a generally positive AR in the highest hypercarbic response slope group. Among the 25 infants having a positive hypercarbic AR, the Mean (± SEM) PACO2at which arousal occurred was 48.5 ± 1.6 in N-M SIDS versus 42 ± 1.2 mmHg in control infants (p < .001). The overall pattern for hypoxic AR was also a generally absent AR in the lowest hypoxic ventilatory response slope group progressing to a generally positive AR in the highest response slope group. Although the PAO2level at which an AR occurred did not differ in the two groups, a positive hypoxic AR occurred in 76% of the control versus only 29% of the N-M SIDS group (p < .01). In summary, infants with a clinical N-M SIDS history and diminished ventilatory response slopes have as a group a concomitant abnormality in hypercarbic and/or hypoxic arousal.
ISSN:0031-3998
出版商:OVID
年代:1981
数据来源: OVID
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