Effects of Hyperoxia on Surfactant Morphology and Cell Viability in Organotypic Cultures of Fetal Rat Lung

Loo, C. K. C.; Smith, Garry J.; Lykke, A. W. J.

doi:10.3109/01902148909069621

Cited by 6 publications

(2 citation statements)

References 26 publications

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“…In contrast. their type 2 cells from newborn rat lungs were comparatively resistant to in vitro hyperoxic exposure (27). In comparing our present survival results in 21-d prematurely delivered rat pups with an earlier in t'il'll report by Tanswell et a/.…”

Section: O -I I I I I I I I I I I I I L 0 1 2 3 4 5 6 7 8 9 1 0 1 1supporting

confidence: 63%

Comparative Responses of Premature Versus Full-Term Newborn Rats to Prolonged Hyperoxia

1994

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ABSTRACT. Because fetal rat lungs have lower baseline levels of both surfactant and antioxidant enzymes than fullterm newborn rats, we questioned whether prematurely delivered rats might be more susceptible to 0 2 toxicity than those born a t term. In the present studies, prematurely delivered rats (gestational d 21 of 22) and full-term rat pups were simultaneously put in >95% O 2 after birth. Surprisingly, we found that the preterm rats were not more susceptible to 02-induced lung damage and lethality than full-term newborns, but, in fact, the composite percentage of survival was even greater in the preterm pups from 7 to 9 d in hyperoxia and were similar thereafter up to 14 d in high 02. In addition, the preterm rats showed significantly decreased lung wetidry weight ratios and consistently less severe pathologic evidence of pulmonary edema compared with term rats at 6 and 8 d of 0 2 exposure. The premature pups demonstrated the capability of inducing pulmonary antioxidant enzyme responses to hyperoxia by 3 d, and had significantly elevated copper-zinc superoxide dismutase, catalase, and glutathione peroxidase activities (and lung surfactant contents) a t 6 d of 0 2 exposure compared with the term rats in 02. The rates of lung total O 2 consumption and cyanide-resistant 0 2 consumption a t d 6 in hyperoxia were not different for preterm versus term pups. Although the basis for the transiently improved survival and decreased evidence of pulmonary 0 2 toxicity in the preterm rats is presently unknown, these findings clearly indicate that premature animals of a t least one species are equally able to induce protective lung antioxidant enzymes and surfactant responses to hyperoxia a s full-term newborn animals. Neonatal animals of many species are relatively resistant to pulmonary oxygen toxicity and lethality when compared with adult animals of the same species ( 1 ). This relative 0 2 tolerance is manifested by much longer survival in hyperoxia and is associated with the induction of increased lung AOE (superoxide dismutase, catalase, and glutathione peroxidase) activities during O2 exposure (1). Augmented AOE activity levels have been consistently associated with protection from hyperoxic exposure, 7and conversely. the failure to increase protective AOE activities during high O2 challenge usually results in susceptibility to severe 02-induced lung damage (and lethality) (2-4).Because fetal rats have lower baseline levels of both surfactant and pulmonary AOE compared with full-term newborn rats (5). we questioned whether premature rats might be more susceptible to O2 toxicity than those born at term. T o answer this experimental question, which to date has been previously explored in only two other species (rabbit and guinea pig). we performed studies in which term-newborn and prematurely delivered rats were simultaneously exposed to prolonged hyperoxia. Comparative AOE and surfactant responses to Oz challenge were determined. as were comparative assessments of 02-induced lung damage. The findings herein indica...

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Section: O -I I I I I I I I I I I I I L 0 1 2 3 4 5 6 7 8 9 1 0 1 1supporting

confidence: 63%

Comparative Responses of Premature Versus Full-Term Newborn Rats to Prolonged Hyperoxia

1994

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“…Holm et al (1985) described a reduced rate of synthesis for PC, a decreased intracellular lipid content, and, as a further parallel to the findings with ozone toxicity, a suppressed activity of the enzyme glycerol-3-phosphate acyltransferase. Enlarged lamellar bodies have also been described (Loo et al 1989) subsequent to in vitro exposure of rat type II pneumocytes. Nogee et al found increased apoprotein recovery (SP-A, SP-B, SP-C) in the lung lavage fluid (LLF) of rats following 1-7 days of exposure to an aerosol containing 85% oxygen (Nogee et al 1991).…”

Section: Effects Of Inhalative Pollutants On the Pulmonary Surfactant...mentioning

confidence: 92%

Does the Pulmonary Surfactant System Yield Meaningful Parameters in Inhalation Toxicity Studies? A Review

Klingebiel

Heinrich

1993

Advances in Controlled Clinical Inhalation Studies

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Pulmonary disease of the newborn

Greenough¹,

Milner²,

Hannam³

et al. 2012

Rennie &Amp; Roberton's Textbook of Neonatology

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Effects of Hyperoxia on Surfactant Morphology and Cell Viability in Organotypic Cultures of Fetal Rat Lung

Cited by 6 publications

References 26 publications

Comparative Responses of Premature Versus Full-Term Newborn Rats to Prolonged Hyperoxia

Comparative Responses of Premature Versus Full-Term Newborn Rats to Prolonged Hyperoxia

Does the Pulmonary Surfactant System Yield Meaningful Parameters in Inhalation Toxicity Studies? A Review

Pulmonary disease of the newborn

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