Suzuki S, Noda M, Sugita M, Ono S, Koike K, Fujimura S
Department of Thoracic Surgery, Institute of Development, Aging, and Cancer, Tohoku University, Aoba-ku, Sendai 980-8575, Japan.
J Appl Physiol (1985). 1999 Sep;87(3):962-8. doi: 10.1152/jappl.1999.87.3.962.
We examined whether hypoxic exposure in vivo would influence transalveolar fluid transport in rats. We found a significant decrease in alveolar fluid clearance of the rats exposed to 10% oxygen for 48 h. Terbutaline did not stimulate alveolar fluid clearance, and alveolar fluid cAMP levels were lower than those determined in normoxia experiment. Hypoxia did not influence the alveolar fluid lactate dehydrogenase levels, Evans blue dye fluid-to-serum concentration ratio, or lung wet-to-dry weight ratio, indicating no significant change in the permeability of alveolar-capillary barrier. Histological examination showed no significant fluid accumulation into the interstitium and the alveolar space. Hypoxia did not reduce lung ATP content; however, we found significant decrease in Na(+)-K(+)-ATPase hydrolytic activity in lung tissue preparations and isolated alveolar type II cells. Our data indicate that hypoxic exposure in vivo impairs transalveolar fluid transport, and this impairment is related to the decrease in alveolar epithelial Na(+)-K(+)-ATPase hydrolytic activity but is not secondary to the alteration of cellular energy source.
我们研究了体内低氧暴露是否会影响大鼠的经肺泡液体转运。我们发现,暴露于10%氧气环境48小时的大鼠,其肺泡液体清除率显著降低。特布他林不能刺激肺泡液体清除,且肺泡液体中环磷酸腺苷(cAMP)水平低于常氧实验中的测定值。低氧并未影响肺泡液体中乳酸脱氢酶水平、伊文思蓝染料的液-血清浓度比或肺湿重与干重比,这表明肺泡-毛细血管屏障的通透性无显著变化。组织学检查显示,间质和肺泡腔内无明显液体蓄积。低氧并未降低肺组织中的三磷酸腺苷(ATP)含量;然而,我们发现肺组织匀浆和分离的肺泡II型细胞中钠钾ATP酶水解活性显著降低。我们的数据表明,体内低氧暴露会损害经肺泡液体转运,这种损害与肺泡上皮钠钾ATP酶水解活性降低有关,但并非继发于细胞能量来源的改变。