肺有双重供血,包括肺动脉和支气管动脉。肺动脉占据肺供血的99%和负责气体交换。支气管动脉仅占肺供血的1%,其营养分支供应支气管,肺动脉和静脉的滋养血管以及发出支气管肺分支到肺实质[1,2]。在支气管和肺小叶水平的肺动脉与支气管动脉形成众多的吻合交通支[1]。这种交通所形成的生理上右到左分流占全部心输出量的近5%[2]。
当肺动脉循环遭到损伤的时候,如低氧性血管狭窄、血管内血栓形成和血管炎,支气管动脉代偿增生,并逐渐替代肺动脉循环[2,3]。肺的慢性炎症也与支气管动脉的代偿相关,导致肺小动脉(pulmonary arterioles )异常交通增加[4,5]。炎症的过程释放血管源性生长因子( angiogenic growth factors),其促进新生血管和来自邻近体循环侧支血管的形成[6]。这些新生的血管壁薄和脆弱,在体循环压力下容易破裂到气道,导致咯血。预计肺泡间隙400ml血量显著抑制气体交换[7],并引起窒息性死亡而不是血容量丢失性死亡[8]。
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