Effect of prenatal isoxsuprine on pulmonary oxygen toxicity in the newborn rat

1980 ◽  
Vol 48 (3) ◽  
pp. 505-510 ◽  
Author(s):  
L. Frank ◽  
J. Summerville ◽  
D. Massaro
Keyword(s):  
Enzyme Activities ◽  
Oxygen Toxicity ◽  
Fetal Lung ◽  
Antioxidant Enzyme Activities ◽  
Newborn Rats ◽  
Lung Maturation ◽  
Lung Weight ◽  
Pregnant Rats ◽  
Rat Pups ◽  
Hyperoxic Exposure

Isoxsuprine, a beta-sympathomimetic agent used clinically to delay premature parturition and to possibly accelerate fetal lung maturation, was administered to pregnant rats at 48 and 24 h prior to delivery. Newborn rats were placed in 96-98% O2 (or room air) to determine if the prenatal isoxsuprine treatment compromised their tolerance to prolonged hyperoxic exposure. (Exogenous catecholamines are known to exacerbate O2 toxicity in adult animals). Survival of the isoxsuprine-treated pups in O2 (52%) was no different than for control neonates exposed to hyperoxia for 7 days (57%) (P = 0.22). Body weight, lung weight, lung protein, and DNA content of the newborns were also not altered by the prenatal isoxsuprine treatment. Lung antioxidant enzyme activities for superoxide dismutase, catalase, and glutathione peroxidase were the same at birth in the isoxsuprine-treated and control rat pups, and the enzyme activities increased in response to hyperoxic exposure in each group to an equivalent degree. Thus, in utero treatment with isoxsuprine had no apparent adverse effect on newborn rats exposed to a prolonged O2 challenge.

Oxygen toxicity in newborn rats: the adverse effects of undernutrition

1982 ◽  
Vol 53 (5) ◽  
pp. 1248-1255 ◽  
Author(s):  
L. Frank ◽  
E. Groseclose
Keyword(s):  
Dna Content ◽  
Oxygen Toxicity ◽  
Lung Damage ◽  
Newborn Rats ◽  
Inhibitory Effects ◽  
Similar Extent ◽  
Newborn Rat ◽  
Lung Maturation ◽  
Rat Pups ◽  
Growth Inhibitory

Undernutrition was found to compromise the tolerance of newborn rat pups to hyperoxia (greater than 95% O2 for 7 days). Survival rate for the normally nourished pups (11 pups/dam) was 56 of 77 (73%) but only 47 of 108 (44%) for the undernourished (18 pups/dam) group (P less than 0.005). Body growth, lung growth, and lung DNA content were significantly reduced by undernutrition. Hyperoxia inhibited these same parameters in both groups of pups. The growth inhibitory effects of O2 and undernutrition were additive, with an especially marked depression of lung DNA content (decreases 65%). Lung maturation was also markedly inhibited by O2 but to a similar extent in both nutrition groups. Despite the disparity in their O2 tolerance, 18/litter and 11/litter pups in O2 responded with equivalent increases in lung antioxidant enzymes. We suggest that the additive depressive effects of neonatal undernutrition and hyperoxia on lung DNA may compromise repair of ongoing O2-induced lung damage and help account for the compromised O2-tolerance we consistently observed even in the presence of significantly elevated antioxidant enzyme defenses.

Oxygen toxicity in neonatal and adult animals of various species

1978 ◽  
Vol 45 (5) ◽  
pp. 699-704 ◽  
Author(s):  
L. Frank ◽  
J. R. Bucher ◽  
R. J. Roberts
Keyword(s):  
Antioxidant Enzyme ◽  
Oxygen Toxicity ◽  
Antioxidant Enzyme Activities ◽  
Defense System ◽  
Exposure System ◽  
Hyperoxic Exposure ◽  
Respective Parent ◽  
Study Support

Neonatal and adult animals of five species were exposed to 95+% O2. Survival time and changes in lung antioxidant enzyme activity (superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GP)) in response to hyperoxia were determined. Adult animals succumbed to O2 lung toxicity in 3--5 days. Neonatal rats, mice and rabbits showed minimal lung changes after 7 days of hyperoxic exposure and these same neonatal animals showed rapid and significant increases in lung antioxidant enzyme activities. In contrast, neonatal guinea pigs and hamsters had no lung antioxidant enzyme response to hyperoxia and these neonates died in 95+% O2 as readily as their respective parent animals. Results from an in vitro hyperoxic exposure system suggest that the lack of enzymic response of the guinea pig (and hamster) neonates to O2 challenge is due to an inherent pulmonary biochemical unresponsiveness rather than to a deficiency of a necessary “serum factor.” The results of this species and age study support the important role of the lung antioxidant enzyme defense system in protection of the lung from O2-induced injury.

scholarly journals Perinatal nicotine exposure impairs ability of newborn rats to autoresuscitate from apnea during hypoxia

1998 ◽  
Vol 85 (6) ◽  
pp. 2066-2074 ◽  
Author(s):  
James E. Fewell ◽  
Francine G. Smith
Keyword(s):  
Sleep Apnea ◽  
Infant Death ◽  
Sudden Infant Death ◽  
Repeated Exposure ◽  
Hypoxic Exposure ◽  
Sudden Infant ◽  
Perinatal Exposure ◽  
Newborn Rats ◽  
Pregnant Rats ◽  
Rat Pups

Failure to autoresuscitate by hypoxic gasping during prolonged sleep apnea has been suggested to play a role in sudden infant death. Furthermore, maternal smoking has been repeatedly shown to be a risk factor for sudden infant death. The present experiments were carried out on newborn rat pups to investigate the influence of perinatal exposure to nicotine (the primary pharmacological and addictive agent in tobacco) on their time to last gasp during a single hypoxic exposure and on their ability to autoresuscitate during repeated exposure to hypoxia. Pregnant rats received either nicotine (6 mg ⋅ kg−1 ⋅ 24 h−1) or vehicle continuously from day 6 of gestation to days 5 or 6 postpartum via an osmotic minipump. On days 5 or 6 postpartum, pups were exposed either to a single period of hypoxia (97% N2-3% CO2) and their time to last gasp was determined, or they were exposed repeatedly to hypoxia and their ability to autoresuscitate from primary apnea was determined. Perinatal exposure to nicotine did not alter the time to last gasp, but it did impair the ability of pups to autoresuscitate from primary apnea. After vehicle, the pups were able to autoresuscitate from 18 ± 1 (SD) periods of hypoxia, whereas, after nicotine, the pups were able to autoresuscitate from only 12 ± 2 periods ( P < 0.001) of hypoxia. Thus our data provide evidence that perinatal exposure to nicotine impairs the ability of newborn rats to autoresuscitate from primary apnea during repeated exposure to hypoxia, such as may occur during episodes of prolonged sleep apnea.

Effects of bacterial endotoxin on protecting copper-deficient rats from hyperoxia

1986 ◽  
Vol 61 (3) ◽  
pp. 982-987 ◽  
Author(s):  
T. H. Spence ◽  
S. G. Jenkinson ◽  
K. H. Johnson ◽  
J. F. Collins ◽  
R. A. Lawrence
Keyword(s):  
Superoxide Dismutase ◽  
Enzyme Activities ◽  
Bacterial Endotoxin ◽  
Antioxidant Enzyme Activities ◽  
Low Doses ◽  
Sod Activity ◽  
Hyperoxic Exposure ◽  
And Control ◽  
Phosphate Buffered Saline ◽  
Increased Susceptibility

The administration of very low doses of bacterial endotoxin protects rats during exposure to hyperoxia and is associated with the induction of lung antioxidant enzyme activities. Copper-deficient rats have increased susceptibility to O2 toxicity, which may be related to their decreased lung superoxide dismutase activity (SOD) or decreased plasma ceruloplasmin concentrations. To determine whether endotoxin can protect against hyperoxia in this susceptible model, we exposed copper-deficient and control rats to a fractional inspiratory concentration of O2 greater than 0.95 for 96 h after pretreatment with 500 micrograms/kg of bacterial endotoxin or phosphate-buffered saline (PBS). Mortality in the copper-deficient and control rats given PBS and exposed to O2 for 96 h was 100%. Copper-deficient rats died significantly earlier during the exposure than controls. No mortality occurred in either group treated with endotoxin and hyperoxia despite the decreased activity of copper-dependent enzymes in the copper-deficient rats. Copper-deficient rats treated with endotoxin and exposed to hyperoxia did increase lung Cu-Zn-SOD activity, but activity remained below levels found in air-exposed controls. Mn-SOD activity was found to be induced above air-exposed controls in the copper-deficient rats treated with endotoxin and exposed to hyperoxia. Hyperoxic exposure resulted in a marked increase in plasma ceruloplasmin concentrations in the control rats, but no increases in ceruloplasmin occurred in the copper-deficient animals. Endotoxin protects copper-deficient rats from hyperoxia despite their decreased lung Cu-Zn-SOD activity, and decreased plasma ceruloplasmin.

Endogenous opioids modulate fetal rabbit lung maturation

1987 ◽  
Vol 62 (6) ◽  
pp. 2141-2146 ◽  
Author(s):  
C. R. Comer ◽  
J. S. Grunstein ◽  
R. J. Mason ◽  
S. C. Johnston ◽  
M. M. Grunstein
Keyword(s):  
Body Weight ◽  
Fetal Lung ◽  
Dry Weight ◽  
Endogenous Opioids ◽  
Opioid Antagonist ◽  
Saline Control ◽  
Lung Maturation ◽  
Rabbit Lung ◽  
Lung Weight ◽  
Air Space

To test the hypothesis that endogenous opioids modulate fetal lung development, separate groups of pregnant rabbits received daily injections of saline, morphine (1 mg/kg body wt), or the opioid antagonist naloxone (0.4 and 5.0 mg) for 10 days during their last trimester of pregnancy. The corresponding groups of fetuses were then delivered prematurely on day 28 of gestation (term approximately 31 days) and evaluated with respect to differences in body weight, lung weight, and the ratios of wet to dry lung weight and lung dry weight to body weight, the static inflation and deflation air and saline pressure-volume (P-V) characteristics of the lungs, and lung morphology. Mean values for body weight, lung weight, and the ratios of lung wet to dry weight and lung dry weight to body weight were not significantly different among the saline control (C), morphine (M)-, and naloxone (NLX)-treated fetuses. On the other hand, the fetal air P-V curves varied significantly (P less than 0.001), wherein the M-treated group depicted increased lung distensibility and alveolar stability on lung deflation, whereas the opposite was obtained in the NLX-treated fetuses. Moreover, morphometric analyses demonstrated that the mean alveolar air space-to-tissue ratio in lungs from M-treated fetuses were significantly greater than that observed either in C or in NLX-treated fetuses (P less than 0.05); however, the air space-to-tissue ratio did not significantly vary between the C and NLX-treated animals. These observations provide new evidence that endogenous opioids enhance fetal lung maturation.

Antioxidant enzyme activities in organ cultures of human fetal lung

1989 ◽  
Vol 17 (4) ◽  
pp. 699-700
Author(s):  
MARY C. McELROY ◽  
FRANK J. KELLY ◽  
ANTHONY D. POSTLE
Keyword(s):  
Antioxidant Enzyme ◽  
Enzyme Activities ◽  
Fetal Lung ◽  
Antioxidant Enzyme Activities ◽  
Organ Cultures ◽  
Human Fetal Lung

Effect of food restriction on hyperoxia-induced lung injury in preterm guinea pig

1992 ◽  
Vol 263 (3) ◽  
pp. L357-L362 ◽  
Author(s):  
S. C. Langley ◽  
F. J. Kelly
Keyword(s):  
Lung Injury ◽  
Guinea Pig ◽  
Antioxidant Enzyme ◽  
Enzyme Activities ◽  
Food Restriction ◽  
Lavage Fluid ◽  
Human Infant ◽  
Antioxidant Defenses ◽  
Antioxidant Enzyme Activities ◽  
Hyperoxic Exposure

Undernutrition may exacerbate hyperoxia-induced lung injury, a finding that may be of significance in the early clinical management of the premature human infant. Addressing this specific problem, we found that 72 h of food restriction in guinea pig pups delivered 3 days preterm increased mortality rates among pups exposed to 95% oxygen (8/18) and yet had no effect on 21% oxygen (air)-exposed pups (0/10). Reduced tolerance of hyperoxic conditions was not, however, associated with increased lung injury, assessed as pulmonary microvascular leakage. Pulmonary antioxidant enzyme activities [Cu,Zn superoxide dismutase (SOD), Mn SOD, glutathione peroxidase, and catalase] were unaltered by starvation or hyperoxia. Lung glutathione concentration was slightly decreased after food restriction, whereas hyperoxic exposure did not change either lung or bronchoalveolar lavage fluid glutathione concentrations or lung antioxidant enzyme activities. Increased susceptibility to the lethal effects of oxygen in the starved preterm guinea pig pup could not be attributed to a deficiency of pulmonary antioxidant defenses.

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