Retarded development of noenatal rat lung by maternal malnutrition.

Curle, D C; Adamson, I. Y. R.

doi:10.1177/26.5.659840

Cited by 34 publications

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“…Starvation of pregnant animals yields smaller fetuses that do not survive parturition or newborns that fail to thrive postnatally (1)(2)(3)(4). Compared with controls, the lungs of starved rat fetuses appear to have reduced septation and delayed surfactant type I1 cell maturation, including the subjective impression of fewer LB in those cells (5). In newborn guinea pigs, the total lung weight, DNA content, alveolar surface area, compliance, and surfactant content are reduced significantly when pregnant animals receive 50% rations of their normal food during the last 3 wk of their 68-d gestation (4,6).…”

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confidence: 99%

Surfactant Content and Type II Cell Development in Fetal Guinea Pig Lungs during Prenatal Starvation

Lin

Lechner

1991

Pediatr Res

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ABSTRACT. Prenatal caloric restriction in guinea pigs causes intrauterine growth retardation and reduced neonatal viability and surfactant phosopholipid (PL). We report here fetal surfactant levels in this model, and correlate total lung PL with ultrastructural maturation of surfactant type I1 cells and lamellar bodies (LB). Pregnant guinea pigs were fed ad libitum throughout their 68-d gestation (control), or fed 50% rations from d 45 until term (starved). Fetal lungs were examined at d 55, 60, and 65 for PL content and composition, including disaturated phosphatidylcholine (DPC), and compared with neonates for both groups. Lung lobes were analyzed ultrastructurally in d 65 fetuses for the numerical, volume, and surface densities of type I1 cells and the volume densities of LB. Prenatal starvation caused significant intrauterine growth retardation at all ages; body and dry lung weights were reduced on d 65 by 26 and 23%, respectively. By d 55 and thereafter, starvation decreased total lung P L by 43-45% but did not alter P L composition. On d 65, the total lung volumes and relative numbers, surface densities, and volumes of type I1 cells in tissue and the relative volumes of LB within type I1 cells did not differ by caloric regimen. Thus, starved and control fetuses had similar total volumes of LB per lung (13-15 pL), although starved animals had significantly less lung DPC. Although the total volume of LB per lung correlated well with total lung DPC from d 55 through birth in controls, starvation led to a significant departure from this relationship. These results suggest that the concentration of DPC within LB can vary markedly without changing the size and appearance of the LB, or that the reduced amounts of DPC in starved fetuses represent deficiencies of surfactant from non-LB compartments. Supported by Grant HL-37386 from the National Heart, Lung, and Blood institute 28 controls, the lungs of starved rat fetuses appear to have reduced septation and delayed surfactant type I1 cell maturation, including the subjective impression of fewer LB in those cells (5). In newborn guinea pigs, the total lung weight, DNA content, alveolar surface area, compliance, and surfactant content are reduced significantly when pregnant animals receive 50% rations of their normal food during the last 3 wk of their 68-d gestation (4, 6).However, the fetal maturation of alveolar type I1 cells after such malnutrition-induced IUGR has never been accurately quantitated in any of these animal models.There are few data on the cellularity of normal human fetal lungs, and none for human hypoplastic lungs caused by or associated with any form of IUGR or prematurity (7). This is despite a mortality rate in neonates weighing ~2 5 0 0 g that is 40 times that of larger neonates during the 1st postnatal month, and that smaller neonates show a higher incidence of neonatal respiratory distress (8,9). Thus, animal models of IUGR may improve current understanding of the pulmonary consequences of similar human intrauterine stress. We have asked two...

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Surfactant Content and Type II Cell Development in Fetal Guinea Pig Lungs during Prenatal Starvation

Lin

Lechner

1991

Pediatr Res

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“…A 4-d fasting in the pregnant rat induced a delay in fetal lung maturation characterized by hypocellularity. diminished PC content, decreased glycogen utilization, and lowered surface active properties of surfactant (3,4). In addition, the incorporation of precursor substrates such as glucose, lactate, and palmitate into fetal lung phospholipids was reduced (5).…”

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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

Guarner¹,

Tordet²,

Bourbon³

1992

Pediatr Res

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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 1 5 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 a t birth (1.70 f 0.31 nmol/mg wet wt versus 3.

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“…Assim, embora acelerem a diferenciação pulmonar, prejudicam a taxa mitótica 31 , inibindo a síntese de DNA 32 , reduzindo o número de células. Entre as alterações teciduais 8,9,15 observadas no desnutrido, que promovem retardo de desenvolvimento pulmonar 33 e diminuição da percentagem de fosfolipídios pulmonares 34 , possivelmente, resulte também a presença de um menor número de receptores de glicocorticóides 35 , atuando como fator limitante no processo 36 . Outras observações, no entanto, levantam a hipótese, em animais com restrição de dieta, que a presença do estresse devido à desnutrição seria capaz de promover aumento de corticói-de circulante, elevando a concentração de fosfolipídios surfactante 37 , através da reutilização de seus componentes, conseqüentemente diminuindo a necessidade de sínte-se de novas moléculas 38 .…”

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Effect of malnutrition and chronic use of nicotine during pregnancy on lung phospholipid concentration in neonate rats

Barbosa¹,

Kopelman²,

Amâncio³

et al. 1999

J Pediatr (Rio J)

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ResumoObjetivo: Avaliar se o uso crônico de nicotina, imposto à rata gestante, independentemente de seu estado nutricional, influencia a concentração de fosfolipídios pulmonares de seus recém-nascidos.Métodos: Oitenta ratas "Wistar EPM-1", após fecundação, e aleatoriamente, foram divididas em 4 grupos controles, que receberam ração normal e água ad libitum e sofreram injeção diária de nenhuma substância, 0,15 ml de solução fisiológica, 900 g/kg de bitartarato de nicotina a 95% e 2.700 g/kg de bitartarato de nicotina a 95%, respectivamente, e em 4 grupos desnutridas, que receberam 13g/dia de ração e água ad libitum e o mesmo tipo de tratamento. No 21º dia de gestação procedeu-se à cesariana, e oitenta recém-nascidos foram selecionados e divididos em 8 grupos de 10 cada, respeitando-se a procedência dos mesmos. Dois pares de pulmões foram extraídos, de cada grupo, para dosagem dos fosfolipídios pulmonares, realizada pelo método de Bartlett.Resultados: Observou-se aumento na concentração de fosfolipídios pulmonares dos recém-nascidos das ratas que não sofreram desnutrição e receberam nicotina, quando comparada com a dos outros grupos.Conclusões: O uso crônico de nicotina, imposto à rata gestante, aumenta a concentração dos fosfolipídios pulmonares nos seus recém-nascidos, e a desnutrição influencia esta concentração. AbstractObjective: The aim of the present study was to determine whether lung phospholipid concentration is affected in neonate rats "Wistar EPM-1" following a continuous 21-day gestational exposure to nicotine.Methods: Eighty rats "Wistar EPM-1" were randomly divided in four control (diet free and water "ad libitum") groups (10 rats each): 1 -Control, 2 -Physiologic Solution (infused with 0.15ml of NaCl 0.9%), 3 -Nicotine 1 (infused with 900 g/kg/day of nicotine bitartrate 95%), and 4 -Nicotine 2 (infused with 2.700 g/kg/day of nicotine bitartrate 95%), and four undernourished (diet 13g/day and water ad libitum) groups (10 rats each), that received the same kind of treatment as the control groups. The infusion of nicotine was subcutaneous. The offspring were divided in eight groups according to their origin.Results: A significant high lung phospholipid concentration was observed in the non-undernourished nicotized group which was injected with a high dose of nicotine. In the other groups, there was no alteration in that concentration.Conclusion: We conclude that gestational exposure to nicotine increases lung phospholipid concentration in neonate rats, and that the nutritional state also influences this lung phospholipid concentration. descritos [1][2][3][4][5][6] , assim como também o impacto da desnutrição da rata grávida sobre seu feto [7][8][9][10] .Diminuição na concentração de fosfolipídios surfactante tem sido verificada em seres humanos fumantes 11 , mas experimentalmente, em animais, no período gestacional, a ação da nicotina sobre a concentração dos fosfolipí-dios pulmonares de seus fetos 12,13 não está ainda bem esclarecida. Assim, este estudo teve o objetivo de avaliar IntroduçãoEfeitos a...

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Retarded development of noenatal rat lung by maternal malnutrition.

Cited by 34 publications

References 0 publications

Surfactant Content and Type II Cell Development in Fetal Guinea Pig Lungs during Prenatal Starvation

Surfactant Content and Type II Cell Development in Fetal Guinea Pig Lungs during Prenatal Starvation

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

Effect of malnutrition and chronic use of nicotine during pregnancy on lung phospholipid concentration in neonate rats

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