Resistance of the pulmonary epithelium to movement of buffer ions
Resistance of the pulmonary epithelium to movement of buffer ions
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DOI：
10.1152/ajplung.00398.2002
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发表时间：
2003-08-01
影响因子：
4.9
通讯作者：
Foss, B
中科院分区：
文献类型：
--
作者：
Effros, RM;Olson, L;Foss, B
据报道，与基底外侧挑战相比，肺泡单层的顶面暴露于酸性和碱性溶液对细胞内pH值的影响很小（Joseph D，Tirmizi O，Zhang X，Crandall艾德和Lubman RL. Am J Physiol Lung Cell Mol Physiol 282：L675-L683，2002）。我们已经使用荧光pH指示剂和三叉光束，以确定是否顶端表面的离子化缓冲液的渗透性比膜分离的血管系统从组织在完整的大鼠肺。在第一组实验中，用含有FITC-葡聚糖（mol wt 60，000）或2 '，7'-双（2-羧乙基）-5（6）-羧基荧光素（BCECF）的灌注液填充空气空间。空气空间pH从7.4逐渐下降至6.61 +/- 0.03（平均值+/- SE，n = 11，空气空间缓冲液为10 mM）。用2 mM NH 4Cl灌注2分钟使空气空间pH增加0.142 +/- 0.019单位，而没有随后的酸性过冲。NaHCO 3和乙酸钠的输注降低了pH值，而没有随后的碱性过冲。在第二组实验中，在用BCECF-AM灌注后在充满空气的肺中监测细胞pH。注射NH 4Cl引起双相反应，最初碱化的细胞室，然后酸化后，NH 4Cl从肺部冲洗。随后的pH值恢复正常的1.0 mM的二甲基阿米洛利的输液减慢。这些研究表明，保护肺细胞免受空气空间酸化的顶膜的不渗透性缓冲离子和细胞挤出多余的H+通过基底侧Na+/H+交换。
Exposure of the apical surfaces of alveolar monolayers to acidic and alkaline solutions has been reported to have little influence on intracellular pH compared with basolateral challenges (Joseph D, Tirmizi O, Zhang X, Crandall ED, and Lubman RL. Am J Physiol Lung Cell Mol Physiol 282: L675-L683, 2002). We have used fluorescent pH indicators and a trifurcated optical bundle to determine whether the apical surfaces are less permeable to ionized buffers than the membranes that separate the vasculature from the tissues in intact rat lungs. In the first set of experiments, the air spaces were filled with perfusate containing FITC-dextran (mol wt 60,000) or 2',7'-bis(2-carboxyethyl)-5(6)-carboxyfluorescein (BCECF). Air space pH fell progressively from 7.4 to 6.61 +/- 0.03 (mean +/- SE, n = 11, air space buffers at 10 mM). Perfusion for 2 min with 2 mM NH4Cl increased air space pH by 0.142 +/- 0.019 unit, without a subsequent acidic overshoot. Infusions of NaHCO3 and sodium acetate reduced pH without a subsequent alkaline overshoot. In the second set of experiments, cellular pH was monitored in air-filled lungs after perfusion with BCECF-AM. Injections of NH4Cl caused a biphasic response, with initial alkalinization of the cellular compartment followed by acidification after the NH4Cl was washed from the lungs. Subsequent return of pH to normal was slowed by infusions of 1.0 mM dimethyl amiloride. These studies suggest that lung cells are protected from air space acidification by the impermeability of the apical membranes to buffer ions and that the cells extrude excess H+ through basolateral Na+/H+ exchangers.