Frank L, Lewis P L, Garcia-Pons T
Pediatr Res. 1985 Mar;19(3):281-6. doi: 10.1203/00006450-198503000-00005.
We used a nutritional deprivation model to produce intrauterine growth-retarded (IGR) rat pups (birth weight = approximately 75% of normal). The IGR newborns evidenced a marked reduction in tolerance to greater than 95% O2 exposure: 10-day survival = 10/47 (21%) versus 18/36 (50%) for control pups, and LT50 = 7.2 days versus 10 days for controls (p less than 0.01). Various lung parameters at birth and during O2 exposure were examined to try to define why prenatal undernutrition should compromise the survival of IGR rats in hyperoxia. We found decreased lung glutathione peroxidase and glucose-6-phosphate dehydrogenase activity (with normal superoxide dismutase and catalase levels) in the IGRs at birth; decreased lung disaturated phosphatidylcholine content (even more markedly decreased in 1-day premature pups); and decreased lung surface area/body weight. These factors and other features of newborn IGRs reported in the literature may help to explain how prenatal undernutrition compromises postnatal tolerance to prolonged high-O2 exposure.
我们采用营养剥夺模型来培育宫内生长受限(IGR)的大鼠幼崽(出生体重约为正常体重的75%)。IGR新生幼崽对大于95%氧气暴露的耐受性显著降低:10天生存率为10/47(21%),而对照幼崽为18/36(50%),半数致死时间(LT50)为7.2天,对照幼崽为10天(p<0.01)。我们检查了出生时及氧气暴露期间的各种肺参数,以试图确定为何产前营养不足会损害IGR大鼠在高氧环境中的生存能力。我们发现,IGR幼崽出生时肺谷胱甘肽过氧化物酶和葡萄糖-6-磷酸脱氢酶活性降低(超氧化物歧化酶和过氧化氢酶水平正常);肺双饱和磷脂酰胆碱含量降低(1日龄早产幼崽中降低更为明显);肺表面积/体重降低。文献中报道的新生IGR的这些因素及其他特征可能有助于解释产前营养不足如何损害产后对长时间高氧暴露的耐受性。