缺氧、内毒素对清醒山羊肺动脉增压反应和肺内液体交换的影响

作者采用山羊慢性肺淋巴瘘模型,观察缺氧、小剂量的内毒素单独及复合作用,对清醒山羊肺动脉压、肺微血管壁通透性及肺组织问液形成的影响。缺氧(模拟4,000m高原,历时5小时)可使肺动脉压显著升高,但肺淋巴流量、淋巴与血浆蛋白比值及肺淋巴蛋白清除率均无明显改变。在平原注射内毒素后其反应可分为三期:(1)肺动脉高压期;(2)肺微血管损伤期;(3)肺微血管壁通透性增高期。在缺氧与内毒素复合作用时,肺动脉压、肺淋巴流量、淋巴与血浆蛋白比值及肺淋巴蛋白清除率的改变,与内毒素单独作用时基本相同。本实验结果提示:(1)缺氧与内毒素复合作用时肺动脉压增高的幅度,并作二者单独作用时幅度的叠加;(2)缺氧不能加重内毒素引起的肺损伤。

Effects of Hypoxia and Endotoxin on Pulmonary Pressor Response and Lung Fluid Exchange in Conscious Goats

The effects of hypoxia and endotoxin, acting alone or in combination, on pulmonary pressor response and lung fluid exchange were studied in 9 conscious goats. Hypoxia(simulating a high altitude of 4,000 m for 5 hours) elevated the pulmonary arterial pressure, but exerted no effect on lung lymph flow, the protein concentration ratio between lymph and plasma, and the clearance rate of lung lymph protein. Three stages were noted after endotoxin injection; the phase of pulmonary hypertension, the phase of pulmonary microvascular injury, and the phase of increased pulmonary microvascular permeability. No obvious difference was observed when endotoxin was acting alone or in combination with hypoxia.The results suggest that 1) the mechanism of pulmonary pressor response induced by hypoxia is somewhat different from that induced by endotoxin, 2)no obvious increase in pulmonary microvascular permeability was noticed during hypobaric hypoxia, and 3) alveolar hypoxia could not enhance the endotoxin-induced lung injury.