Wang C Z, Li A, Zhu P F, Yang Z C, Gao J Y, Zeng S Q, Wang D, An N
Burns Incl Therm Inj. 1986 Aug;12(6):415-21. doi: 10.1016/0305-4179(86)90037-9.
Chronic lung lymph fistulae were produced in six goats according to Winn's and Stothert's methods with our modification to define the pathophysiology of pulmonary oedema after severe steam inhalation injury. Arterial blood gas, lung lymph flow (QLym), lymph/plasma total protein concentration ratio (L/P), and beta-glucuronidase (beta-G) in plasma and lung lymph were monitored for 24 h post-injury. The pathological changes in the lung tissues were also determined at the end of the study. It was found that directly after injury, QLym increased steadily to a peak value at 6 h, followed by declining values at 18 and 24 h. L/P decreased promptly during the 60 min after injury and then also steadily increased to a peak value at 4 h (P less than 0.05). A significant increase in plasma beta-G was only observed at 4 h post-burn. However, lung lymph beta-G activities and lymph beta-G transport increased immediately after injury, reaching a peak at 4 h (5 and 12 times above baseline values, respectively, P less than 0.01). Significant hypoxaemia and hypocapnia occurred at 2 h post-burn and deteriorated progressively throughout the study. There were obvious pulmonary interstitial and alveolar oedema microscopically. This study demonstrates that the increase in transvascular fluid and protein flux after steam inhalation injury is mainly due to increased pulmonary microvascular permeability. Nevertheless, a hydrostatic pressure effect can not be completely excluded, especially in the first hour post-burn. Lysosomal enzyme release is considered to be one of the important factors which damage lung microvascular elements and induce an increase in their permeability.
根据温恩(Winn)和斯托瑟特(Stothert)的方法并加以改进,对六只山羊造成慢性肺淋巴瘘,以明确严重蒸汽吸入性损伤后肺水肿的病理生理学机制。在损伤后24小时监测动脉血气、肺淋巴流量(QLym)、淋巴/血浆总蛋白浓度比(L/P)以及血浆和肺淋巴中的β-葡萄糖醛酸酶(β-G)。在研究结束时还确定了肺组织的病理变化。结果发现,损伤后即刻,QLym稳步增加,在6小时达到峰值,随后在18小时和24小时下降。L/P在损伤后60分钟内迅速下降,然后也稳步增加,在4小时达到峰值(P<0.05)。仅在烧伤后4小时观察到血浆β-G显著增加。然而,肺淋巴β-G活性和淋巴β-G转运在损伤后立即增加,在4小时达到峰值(分别比基线值高5倍和12倍,P<0.01)。烧伤后2小时出现明显的低氧血症和低碳酸血症,且在整个研究过程中逐渐恶化。显微镜下可见明显的肺间质和肺泡水肿。本研究表明,蒸汽吸入性损伤后跨血管液体和蛋白质通量的增加主要是由于肺微血管通透性增加。然而,不能完全排除静水压效应,尤其是在烧伤后的第一小时。溶酶体酶释放被认为是损伤肺微血管成分并导致其通透性增加的重要因素之一。