Factor P, Ridge K, Alverdy J, Sznajder J I
Pulmonary and Critical Care Medicine, Evanston Northwestern Healthcare, Evanston 60201, Illinois, USA.
J Appl Physiol (1985). 2000 Nov;89(5):1759-65. doi: 10.1152/jappl.2000.89.5.1759.
Adult rats exposed to hyperoxia develop anorexia, weight loss, and a lung injury characterized by pulmonary edema and decreased lung liquid clearance. We hypothesized that maintenance of nutrition during hyperoxia could attenuate hyperoxia-induced pulmonary edema. To test this hypothesis, we enterally fed adult male Sprague-Dawley rats via gastrostomy tubes and exposed them to oxygen (inspired O(2) fraction >0.95) for 64 h. In contrast to controls, enterally fed hyperoxic animals did not lose weight and had smaller pleural effusions and wet-to-dry weight ratios (a measure of lung edema) that were not different from room air controls. Enterally fed rats exposed to hyperoxia had increased levels of mRNA for the Na(+)-K(+)-ATPase alpha(1)- and beta(1)-subunits and glutathione peroxidase. These findings suggest that maintenance of nutrition during an oxidative lung injury reduces lung edema, perhaps by allowing for continued expression and function of protective proteins such as the Na(+)-K(+)-ATPase.
成年大鼠暴露于高氧环境会出现厌食、体重减轻以及以肺水肿和肺液清除率降低为特征的肺损伤。我们推测,在高氧环境下维持营养可减轻高氧诱导的肺水肿。为验证这一假设,我们通过胃造瘘管对成年雄性斯普拉格 - 道利大鼠进行肠内喂养,并将它们暴露于氧气(吸入氧分数>0.95)环境中64小时。与对照组相比,经肠内喂养的高氧动物体重未减轻,胸腔积液较少,湿干重比(肺水肿的一项指标)与室空气对照组无异。暴露于高氧环境的经肠内喂养大鼠,其钠钾ATP酶α1和β1亚基以及谷胱甘肽过氧化物酶的mRNA水平升高。这些发现表明,在氧化性肺损伤期间维持营养可减轻肺水肿,可能是通过使诸如钠钾ATP酶等保护性蛋白持续表达并发挥功能来实现的。