Lifshitz F, Wapnir R A, Teichberg S
Proc Soc Exp Biol Med. 1986 Jan;181(1):87-97. doi: 10.3181/00379727-181-42228.
Hypoxia was induced by exposing rats to an atmosphere of 93% N2, 7% O2 for 4-48 hr. The animals became hypoxic as indicated by a decreased blood PaO2 (mean +/- SEM: 48 +/- 10 mm Hg). Hypoxia was accompanied by metabolic acidosis (pH 7.22 +/- 0.02) and decreased serum bicarbonate levels (9.0 +/- 4.0 meq/liter). Hypoxic rats also showed evidence of tissue hypoxia; liver tryptophan oxygenase levels were increased to 21 +/- 2 nmole/min/mg protein. In the hypoxic animals there was decreased jejunal mucosal (Na+-K+)-ATPase activity and an inhibition of active intestinal transport of sodium, glucose, 3-O-methylglucose, galactose, tyrosine, phenylalanine, and glycine as determined by in vivo perfusion studies. Jejunal fructose transport, which has a large passive component, was unaffected by hypoxia. The electrolyte, carbohydrate, and amino acid transport alterations produced by hypoxia were seen in the absence of an effect on jejunal cell number, DNA synthesis, or cell turnover. There was also no evidence of histological or ultrastructural damage. Furthermore, studies with a luminal macromolecular tracer, horseradish peroxidase, indicated that the jejunal lumen-to-blood barrier to macromolecules was also unaltered in these hypoxic animals. In vitro local oxygenation of the jejunum, by bubbling of 95% O2:5% CO2, markedly improved sodium and glucose (but not 3-O-methylglucose) absorption in hypoxic rats and control rats. The (Na+-K+)-ATPase activity of the jejunal mucosa of hypoxic rats was significantly enhanced by the local bubbling of 95% O2:5% CO2. Overall, our data indicate that during relatively mild conditions of hypoxia there is an inhibition of jejunal (Na+-K+)-ATPase activity and related transport processes that is prevented by in situ oxygenation.
通过将大鼠暴露于含93% N₂、7% O₂的环境中4 - 48小时来诱导缺氧。如血液中动脉血氧分压降低（平均值±标准误：48±10 mmHg）所示，动物出现了缺氧症状。缺氧伴随着代谢性酸中毒（pH 7.22±0.02）和血清碳酸氢盐水平降低（9.0±4.0 meq/升）。缺氧大鼠还表现出组织缺氧的迹象；肝脏色氨酸加氧酶水平增加到21±2 nmol/分钟/毫克蛋白。在缺氧动物中，空肠黏膜（Na⁺-K⁺）-ATP酶活性降低，并且通过体内灌注研究确定，钠、葡萄糖、3 - O - 甲基葡萄糖、半乳糖、酪氨酸、苯丙氨酸和甘氨酸的肠道主动转运受到抑制。空肠果糖转运具有较大的被动成分，不受缺氧影响。在对空肠细胞数量、DNA合成或细胞更新无影响的情况下，观察到了缺氧引起的电解质、碳水化合物和氨基酸转运改变。也没有组织学或超微结构损伤的证据。此外，使用腔内大分子示踪剂辣根过氧化物酶的研究表明，在这些缺氧动物中，空肠腔到血液的大分子屏障也未改变。通过向空肠局部鼓入95% O₂:5% CO₂进行体外局部氧合，可显著改善缺氧大鼠和对照大鼠对钠和葡萄糖（但不是3 - O - 甲基葡萄糖）的吸收。通过向空肠局部鼓入95% O₂:5% CO₂，缺氧大鼠空肠黏膜的（Na⁺-K⁺）-ATP酶活性显著增强。总体而言，我们的数据表明，在相对轻度的缺氧条件下，空肠（Na⁺-K⁺）-ATP酶活性及相关转运过程受到抑制，而原位氧合可防止这种抑制。
