TNF-alpha in smoke inhalation lung injury
TNF-alpha in smoke inhalation lung injury
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DOI：
10.1152/jappl.1997.82.5.1433
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发表时间：
1997-05-01
影响因子：
3.3
通讯作者：
Efimova, O
中科院分区：
文献类型：
--
作者：
Hales, CA;Elsasser, TH;Efimova, O
成人呼吸窘迫综合征是火灾受害者发病的主要原因。肿瘤坏死因子-α(TNF-α)是水肿性的，与其他形式的成人呼吸窘迫综合征的病因有关。在绵羊淋巴瘘模型中，我们测定了吸入棉花烟48(n=7)或128(n=3)后的肿瘤坏死因子-α，并将其与假手术对照组(n=5)或对照组(n=5)进行比较，在没有炎症的情况下将左房压力升高至20 mm Hg以增加淋巴流量。吸烟导致淋巴流量和肺动脉压升高，淋巴-血浆蛋白比率(128次呼吸)没有下降，淋巴-血浆蛋白比率(48次呼吸)略有下降，这与微血管通透性的变化和微血管压力的上升一致。两组淋巴中的肿瘤坏死因子-α浓度均下降，但淋巴流量(浓度x流量)均有一过性升高。在这两种情况下，肿瘤坏死因子-α都没有。流量超过左房内压升高时的流量。在肺泡灌洗中，只有五分之一的绵羊检测到了肿瘤坏死因子-α。因此，通过使用灵敏和特异的放射免疫分析，我们不能证明肿瘤坏死因子-α在烟雾诱导的绵羊微血管肺损伤中的作用。
Adult respiratory distress syndrome is a major cause of morbidity in fire victims. Tumor necrosis factor-alpha (TNF-alpha) is edematogenic and has been associated with the etiology of other forms of adult respiratory distress syndrome. In the sheep lymph fistula model, we measured TNF-alpha after 48 (n = 7) or 128 (n = 3) breaths of cotton smoke and compared this with sham controls (n = 5) or controls in which left atrial pressure was elevated to 20 mmHg (n = 5) to increase lymph flow in the absence of inflammation. Smoke induced a rise in lymph flow and pulmonary arterial pressure with either no fall in lymph-to-plasma protein ratio (128 breaths) or a modest fall in lymph-to-plasma protein ratio (48 breaths), consistent with a change in microvascular permeability as well as a rise in microvascular pressure. Lymph concentration of TNF-alpha fell in both groups, although lymph flux (concentration x flow) transiently rose in both. In neither case did TNF-alpha. flux exceed that induced by left atrial pressure elevation. TNF-alpha was detectable in only one out of five sheep in alveolar lavage. Thus, by utilizing a sensitive and specific radioimmunoassay, we were unable to demonstrate a role for TNF-alpha in smoke-induced microvascular lung injury in sheep.