Intrauterine Growth-Retarded Rat Pups Show Increased Susceptibility to Pulmonary O2 Toxicity

Frank, Lee; Lewis, Pamela; Garcia-Pons, Teresa

doi:10.1203/00006450-198503000-00005

Cited by 16 publications

(10 citation statements)

References 17 publications

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“…The growth pattern noted in our STZ offspring is similar to that recently described for intrauterine growth-retarded rats, produced by maternal nutritional deprivation (27). Since our maternal STZ rats lost rather than gained weight during pregnancy, presumably due to their chemically induced hypoinsulin state, the STZ offspring may also have been exposed to relative maternal malnutrition.…”

Section: Dspc and Antioxidant Enzymes In The Idmsupporting

confidence: 57%

Lung Development in the Streptozotocin Rat Fetus: Antioxidant Enzymes and Survival in High Oxygen

Sosenko

Frank

1986

Pediatr Res

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ABSTRACT. Offspring of experimentally induced diabetic DSPC, disaturated phosphatidylcholine animals demonstrate delays in functional, biochemical, and Lm, mean linear intercept morphological aspects of lung maturation, dealing mainly with the surfactant system. To investigate whether the development of the lung antioxidant enzyme system would be similarly delayed, and thus compromise their tolerance to high O2 exposure, we did the following: 1) produced the diabetic state in rats with streptozotocin injection 24 h after the onset of pregnancy; 2) examined fetal animals from streptozotocin and control rats at gestational days 19, 20, and 21, and newborn animals at day 22 for whole lung disaturated phosphatidylcholine and total phospholipid and for the three antioxidant enzymes: superoxide dismutase, catalase, glutathione peroxidase; and 3) exposed newborn offspring from steptozotocin-treated and control rats to >95% O2 for several days and their survival, changes in antioxidant enzymes and disaturated phosphatidylcholine and light microscopic findings in response to hyperoxic challenge were compared. Streptozotocin offspring demonstrated essentially no developmental differences in whole lung disaturated phosphatidylcholine, total phospholipid, or antioxidant enzymes activity at the 4 gestational days studied. However, newborns of streptozotocin mothers had consistently superior tolerance to hyperoxic exposure, consisting of increased survival 123134 (68%) versus 8/26 (31%) in controls, after 02-exposure for 13 days, p < 0.0011, microscopic evidence of reduced inhibition of alveolarization (p < 0.05), and a trend toward greater antioxidant enzymes response. Thus, in this animal model of experimental diabetes, neither the development of the antioxidant enzymes system nor the development of the surfactant system (as assessed by whole lung disaturated phosphatidylcholine and total phospholipid) appear delayed. However, the superior tolerance to hyperoxic exposure in streptozotocin offspring raises the question whether maternal diabetes might actually have a protective influence against 02-induced lung damage in prematurely delivered infants of diabetic mothers. IDM have a 6-fold increased risk of developing HMD compared to infants whose mothers are not diabetic (1). This increase in HMD has been attributed to a delay in lung maturation in the IDM. Numerous animal studies both in vivo and in vitro have reported delays in functional, biochemical, and morphological lung development in the IDM, focusing mainly on the surfactant system and the differentiation of the type I1 epithelial cell (2-7). Those infants of diabetic mothers who develop HMD usually require treatment with increased concentrations of inspired oxygen. The antioxidant enzyme system of the lung, consisting in part of superoxide dismutase, catalase, and glutathione peroxidase, is an important defense against free radicals and other toxic O2 metabolites produced intracellularly in excess amounts during exposure to hyperoxia. The development of the pulmonar...

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Section: Dspc and Antioxidant Enzymes In The Idmsupporting

confidence: 57%

Lung Development in the Streptozotocin Rat Fetus: Antioxidant Enzymes and Survival in High Oxygen

Sosenko

Frank

1986

Pediatr Res

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“…These clinical results are supported by experimental data about malnutrition-induced adverse pulmonary effects during the perinatal period. 25,26 Antenatal steroid therapy was not correlated with a lower incidence of COD in univariate analysis. We believe that the beneficial effects of antenatal steroid therapy on COD would have been demonstrated if the rate of treatment has been clearly higher.…”

Section: Discussionmentioning

confidence: 88%

Chronic Oxygen Dependency in Infants Born at Less Than 32 Weeks' Gestation: Incidence and Risk Factors

et al. 2001

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ABSTRACT. Objective. To assess incidence and clinical risk factors of chronic oxygen dependency (COD) among survivors who were born at or before 31 weeks' gestation.Methods. This prospective, multicenter study enrolled 802 infants who were born at or before 31 weeks' gestation and admitted to 8 level III neonatal intensive care units in northern and eastern France from January 1 through December 31, 1997. Need for oxygen to maintain oxygen saturation between 92% and 96% was assessed at 28 days of life and at 36 and 42 weeks' postconceptional age (PCA). Stepwise logistic regression analysis was used to identify the incidence of COD and the risk factors related to its occurrence.Results. The mortality rate was 14%. Antenatal corticotherapy was administered to 51% of patients, surfactant therapy to 76% of the ventilated patients, and highfrequency oscillatory ventilation at day 1 to 32%. At 28 days and 36 and 42 weeks' PCA, respectively, 25%, 15%, and 6% of survivors had COD. After adjustment for intercenter variations, we identified the significant risk factors for COD at these dates: a low gestational age, a high score on the Clinical Risk Index for Infants, intrauterine growth restriction, and surfactant treatment.Conclusion. COD incidence was high at 28 days of life but decreased dramatically by 42 weeks' PCA. This study confirmed previously reported risk factors and underlined the importance of intrauterine growth restriction and the Clinical Risk Index for Infants as significant risk factors. Pediatrics 2001;108(2). URL: http://www. pediatrics.org/cgi/content/full/108/2/e26; bronchopulmonary dysplasia, chronic oxygen dependency.

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“…When exposed to hyperoxia, the newborn rats had decreased lung DNA and glutathione [17] . Similarly, in the premature guinea pig, starvation increased mortality with hyperoxia and there was a decrease in lung and liver glutathione content [18] suggesting the importance of glutathione reduction associated with undernutrition and its role in hyperoxiainduced lung injury.…”

Section: Undernutrition and Lung Injurymentioning

confidence: 99%

Nutrition and the Lung

Bhatia

Parish²

2009

Neonatology

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The use of surfactant replacement, ‘kinder gentler’ modes of ventilation combined with prenatal corticosteroids have all played a role in improved survival rates of very-low-birth-weight infants but have not reduced the prevalence of chronic lung disease. The increased rates of prematurity being observed in the United States along with the increased survival makes the overall problem of treatment of infants with established disease expensive spanning neonatology, pediatric critical care and general pediatrics and involving a myriad of specialists over the life of the surviving infant. However, none of the therapies used over the years have proven to be effective or have long-term adverse effects, nor have they been accepted as methods to prevent chronic lung disease. Although intuitively an appropriate nutritional therapy may be a useful adjunct in the care of the premature sick infant, perinatal malnutrition remains a major problem. The role of nutrition therapy in health and disease as it pertains to the lung will be reviewed.

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Intrauterine Growth-Retarded Rat Pups Show Increased Susceptibility to Pulmonary O2 Toxicity

Cited by 16 publications

References 17 publications

Lung Development in the Streptozotocin Rat Fetus: Antioxidant Enzymes and Survival in High Oxygen

Lung Development in the Streptozotocin Rat Fetus: Antioxidant Enzymes and Survival in High Oxygen

Chronic Oxygen Dependency in Infants Born at Less Than 32 Weeks' Gestation: Incidence and Risk Factors

Nutrition and the Lung

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