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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。
The authors used a goat chronic lung lymphatic fistula model to observe the effect of hypoxia and low-dose endotoxin alone and in combination on pulmonary arterial pressure, pulmonary microvascular permeability and pulmonary fluid formation in conscious goats. Hypoxia (simulated 4,000 m plateau for 5 hours) significantly increased pulmonary arterial pressure, but no significant changes were observed in the lung lymphatic flow, lymphoid to plasma protein ratio, and lung lymph protein clearance. After the endotoxin injection in the plain its response can be divided into three phases: (1) pulmonary hypertension period; (2) lung microvascular injury; (3) pulmonary microvascular permeability increased. In the combination of hypoxia and endotoxin, pulmonary arterial pressure, pulmonary lymph flow, lymph and plasma protein ratio and lung lymph protein clearance changes, and endotoxin alone is basically the same. The results suggest that: (1) hypoxia and endotoxin combined effect of pulmonary artery pressure increased amplitude, and for the two when the amplitude of the role of the superposition; (2) hypoxia can not aggravate endotoxin-induced lung injury.