Mullins R J
J Surg Res. 1986 Jun;40(6):540-9. doi: 10.1016/0022-4804(86)90096-x.
Bradykinin is an endogenous inflammatory mediator, and its mechanism of action is incompletely understood. It is controversial whether bradykinin causes a sustained increase in microvascular permeability, or has only a transient effect. In anesthetized dogs intraarterial infusion of bradykinin (0.14 to 0.54 micrograms/kg/min) produced an immediate increase in flow of protein-rich, hindpaw lymph. After 210 min of bradykinin infusion lymph flow was threefold greater than baseline, lymph protein concentration remained doubled, and in a dose-related fashion bradykinin produced a sustained increase in lymph protein flux. Lymph flow was then further increased with venous hypertension, and after 4 hr lymph protein flux remained greater from the bradykinin paws than from the control paws. This sustained increase in protein flux indicates that bradykinin produces an increase in permeability at the microvascular membrane by a mechanism that is different from how the initial increase in permeability was produced.
缓激肽是一种内源性炎症介质,其作用机制尚未完全明确。缓激肽是否会导致微血管通透性持续增加,还是仅具有短暂效应,这一点存在争议。在麻醉犬中,动脉内输注缓激肽(0.14至0.54微克/千克/分钟)可使富含蛋白质的后爪淋巴液流量立即增加。输注缓激肽210分钟后,淋巴液流量比基线增加了两倍,淋巴蛋白浓度仍翻倍,并且缓激肽以剂量相关的方式使淋巴蛋白通量持续增加。然后通过静脉高压进一步增加淋巴液流量,4小时后,缓激肽处理的爪子的淋巴蛋白通量仍高于对照爪子。这种蛋白通量的持续增加表明,缓激肽通过一种不同于最初通透性增加的机制,使微血管膜的通透性增加。