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母体蛋白质-热量营养不良对从胎鼠和新生鼠肺中分离出的表面活性剂磷脂成分的影响。肌醇和脂质补充的补偿作用。

Effects of maternal protein-calorie malnutrition on the phospholipid composition of surfactant isolated from fetal and neonatal rat lungs. Compensation by inositol and lipid supplementation.

作者信息

Guarner V, Tordet C, Bourbon J R

机构信息

Centre de Biologie Cellulaire, Centre National de la Recherche Scientifique, Ivry-sur-Seine, France.

出版信息

Pediatr Res. 1992 Jun;31(6):629-35. doi: 10.1203/00006450-199206000-00018.

Abstract

The effects of a maternal protein-calorie malnutrition during gestation and lactation were analyzed on fetal and postnatal lung growth and maturation, including a surfactant fraction isolated from lung tissue. There was a considerable reduction in body weight and in wet and dry lung weights of malnourished pups. Lung protein and DNA concentrations were similar in both groups except in late gestation (lung hyperplasia) and 2 and 15 d after delivery (hypocellularity). Lung glycogen breakdown was slowed down in malnourished newborns. Surfactant material was decreased the most perinatally and the reduction was more marked than for the nonsurfactant fraction of the lung. Disaturated phosphatidylcholine, the major surface active surfactant component, was decreased the most at birth (1.70 +/- 0.31 nmol/mg wet wt versus 3.68 +/- 0.17 nmol/mg in controls, n = 8) and on d 2 (5.04 +/- 0.53 nmol/mg versus 7.67 +/- 0.44 nmol/mg in controls, n = 8). There was an apparent recovery in the composition of surfactant in malnourished rats 5 d after delivery, due in fact to a decrease in controls, and an actual return to normal levels 15 to 20 d after birth. Postnatal lipid supplementation with Intralipid led to partial recovery on d 10. Inositol supplementation totally reverted the effects of malnutrition on surfactant phospholipids (8.36 +/- 0.94 nmol disaturated phosphatidylcholine/mg wet wt on d 2 versus 7.67 +/- 0.44 nmol/mg in controls and 5.55 +/- 0.62 nmol/mg in untreated malnourished rats, n = 10; 2.43 +/- 0.32 nmol disaturated phosphatidylcholine/mg wet wt on d 10 versus 3.26 +/- 0.32 nmol/mg in controls and 1.18 +/- 0.27 nmol/mg in untreated malnourished rats, n = 8).(ABSTRACT TRUNCATED AT 250 WORDS)

摘要

分析了孕期和哺乳期母体蛋白质 - 热量营养不良对胎儿及出生后肺生长和成熟的影响,包括从肺组织分离出的表面活性剂成分。营养不良幼崽的体重以及肺的湿重和干重显著降低。除了在妊娠晚期(肺增生)以及出生后2天和15天(细胞减少)外,两组的肺蛋白质和DNA浓度相似。营养不良新生儿的肺糖原分解减缓。表面活性物质在围产期减少最多,且减少程度比肺的非表面活性物质部分更明显。主要的表面活性表面活性剂成分二饱和磷脂酰胆碱在出生时减少最多(1.70±0.31 nmol/mg湿重,对照组为3.68±0.17 nmol/mg,n = 8),在出生后第2天也是如此(5.04±0.53 nmol/mg,对照组为7.67±0.44 nmol/mg,n = 8)。营养不良大鼠在出生后5天,表面活性剂成分明显恢复,实际上是由于对照组减少,而在出生后15至20天实际恢复到正常水平。出生后用英脱利匹特补充脂质在第10天导致部分恢复。补充肌醇完全逆转了营养不良对表面活性剂磷脂的影响(出生后第2天,8.36±0.94 nmol二饱和磷脂酰胆碱/mg湿重,对照组为7.67±0.44 nmol/mg,未治疗的营养不良大鼠为5.55±0.62 nmol/mg,n = 10;出生后第1天,2.43±0.32 nmol二饱和磷脂酰胆碱/mg湿重,对照组为3.26±0.32 nmol/mg,未治疗的营养不良大鼠为1.18±0.27 nmol/mg,n = 8)。(摘要截选至250字)

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