Persson C G, Erjefält I, Gustafsson B, Luts A
Department of Clinical Pharmacology, University Hospital of Lund, Sweden.
Int Arch Allergy Appl Immunol. 1990;92(2):148-53. doi: 10.1159/000235206.
This study demonstrated in guinea pig tracheal tubes in vitro that small increases in serosal hydrostatic pressure caused significant mucosal crossing of serosal macromolecules. Reversibility and repeatability of this passage agree with inflammatory stimulus-induced appearance of exuded plasma in airway lumen in vivo. Bradykinin, histamine, and terbutaline, which induce and inhibit, respectively, plasma exudation in vivo, were without effect on the present in vitro permeability. Carbachol, similar to histamine, contracted the trachea, and did not increase, but rather decreased the pressure-induced luminal entry of serosal macromolecules. It is proposed that a plasma-exudation-induced hydrostatic pressure load transiently separates epithelial cells, providing a direction-selective and non-injurious intercellular pathway for passage of bulk plasma exudate into the airway lumen. This mechanism would allow potent plasma protein systems to operate on mucosal surfaces at sites of insults without compromising the mucosa as a barrier to luminal solutes.
本研究在豚鼠气管体外实验中表明，浆膜流体静压的小幅增加会导致浆膜大分子显著穿过黏膜。这种穿过的可逆性和可重复性与体内炎症刺激诱导的气道腔内渗出血浆的出现相一致。在体内分别诱导和抑制血浆渗出的缓激肽、组胺和特布他林，对目前的体外通透性没有影响。与组胺类似，卡巴胆碱使气管收缩，并没有增加，反而降低了压力诱导的浆膜大分子进入管腔。有人提出，血浆渗出诱导的流体静压负荷会暂时分离上皮细胞，为大量血浆渗出物进入气道腔提供一个方向选择性且无损伤的细胞间通道。这种机制将允许有效的血浆蛋白系统在损伤部位的黏膜表面发挥作用，而不会损害黏膜作为管腔溶质屏障的功能。
