Al-Bazzaz F J
Clin Chest Med. 1986 Jun;7(2):259-72.
Effective mucociliary clearance of secretions by airway mucosa requires efficient ciliary beating. The structure of airway secretions provides for this requirement by having a viscous mucous layer touched underneath and propelled by ciliary tips, while the rest of the cilium is surrounded by a serous fluid layer. The regulation of the latter layer is thought to be a function of mucosal epithelial cells capable of active ion transport. Mammalian medium-sized bronchi actively absorb sodium, whereas the tracheal mucosae of several mammals are capable of sodium absorption as well as chloride secretion. By generating local osmotic gradients, these ion transport processes may regulate the depth of the periciliary sol layer. These transport processes generate an electrical PD across the mucosa such that the luminal side is negatively charged in reference to the submucosal side (electrogenic transport). Transport of sodium and chloride across the plasma membrane is against a steep electrochemical gradient, and cellular energy resources are utilized for this purpose (active transport). Chloride transport is coupled to sodium transport; therefore, inhibition of the sodium pump (Na-K-ATPase) with ouabain leads to inhibition of sodium as well as chloride transport. Several neurohumoral agents have been found to stimulate chloride secretion, such as PGs, beta-adrenergic agonists, VIP, substance P, and bradykinin. Mechanisms of regulation of sodium transport by airway epithelia are not clearly understood. Available evidence suggests that elevation of cellular PGs, cAMP, and calcium enhances apical cell-membrane conductance to chloride ion, with an opposite effect on sodium conductance. Therefore, it seems reasonable to suggest that neurohumoral control mechanisms may switch from sodium and fluid absorption to chloride and fluid secretion, and vice versa. Several lines of evidence support this proposal. First, the lung of fetal lamb secretes chloride and fluid in utero; this activity ceases at birth, when the catecholamine level is increased, causing a decrease in chloride secretion. In contrast, adult sheep trachea absorbs sodium. Second, agents that stimulate chloride secretion in bovine trachea concomitantly reduce sodium absorption, and vice versa. Similar observations were noted in some instances in dog trachea. Third, whereas unstimulated ferret and cat tracheas only absorb sodium, they secrete chloride upon exposure to beta agonists.(ABSTRACT TRUNCATED AT 400 WORDS)
气道黏膜对分泌物进行有效的黏液纤毛清除需要有效的纤毛摆动。气道分泌物的结构通过以下方式满足这一需求:下方有一层黏性黏液层,由纤毛尖端触碰并推动,而纤毛的其余部分则被浆液层包围。浆液层的调节被认为是能够进行主动离子转运的黏膜上皮细胞的功能。哺乳动物的中型支气管积极吸收钠,而几种哺乳动物的气管黏膜既能吸收钠,也能分泌氯。通过产生局部渗透梯度,这些离子转运过程可能调节纤毛周围溶胶层的深度。这些转运过程在黏膜上产生一个电动力势,使得管腔侧相对于黏膜下层带负电荷(电生电转运)。钠和氯跨质膜的转运是逆着陡峭的电化学梯度进行的,为此需要利用细胞能量资源(主动转运)。氯的转运与钠的转运相偶联;因此,用哇巴因抑制钠泵(Na-K-ATP酶)会导致钠和氯的转运均受到抑制。已发现几种神经体液因子可刺激氯的分泌,如前列腺素、β-肾上腺素能激动剂、血管活性肠肽、P物质和缓激肽。气道上皮对钠转运的调节机制尚不清楚。现有证据表明,细胞内前列腺素、环磷酸腺苷和钙的升高会增强顶端细胞膜对氯离子的电导,而对钠电导有相反的影响。因此,有理由认为神经体液控制机制可能从钠和液体吸收转变为氯和液体分泌,反之亦然。有几条证据支持这一观点。首先,胎羊的肺在子宫内分泌氯和液体;出生时这种活动停止,此时儿茶酚胺水平升高,导致氯分泌减少。相反,成年绵羊的气管吸收钠。其次,刺激牛气管中氯分泌的因子会同时减少钠的吸收,反之亦然。在狗的气管中,某些情况下也有类似的观察结果。第三,未受刺激的雪貂和猫的气管只吸收钠,但在接触β激动剂后会分泌氯。(摘要截选至400字)