Traber D L, Hawkins H K, Enkhbaatar P, Cox R A, Schmalstieg F C, Zwischenberger J B, Traber L D
The Investigative Intensive Care Unit, The University of Texas Medical Branch and Shrine Hospital For Children, 300 University Blvd., Galveston, TX 77555-0833, USA.
Pulm Pharmacol Ther. 2007;20(2):163-6. doi: 10.1016/j.pupt.2005.12.006. Epub 2006 Jun 22.
Smoke inhalation in burn patients is a serious medical problem around the world. Inhalation injury increases mortality in addition to increasing infections, ventilator-days, and hospital stays. There are also large numbers of patients subjected to smoke inhalation without burns from cooking fires, burning crops and forest fires. The injury results in a fall in arterial oxygenation as a result of airway blockade, increased pulmonary transvascular fluid flux and loss of hypoxic pulmonary vasoconstriction. The changes in cardiopulmonary function are mediated at least in part by reactive oxygen and nitrogen species. Nitric oxide (NO) is generated by both inducible and constitutive isoforms of nitric oxide synthase (NOS). NO combines with superoxide to form reactive nitrogen species such as peroxynitrite. These reactive nitrogen species can be detected by measuring their reaction products such as 3-nitrotyrosine. The latter is elevated in the airway following smoke/burn injury. The control of NO formation involves poly (ADP ribose) polymerase (PARP) and its ability to up-regulate the activity of nuclear transcription factors through ribosylation. Present data also support a major role for the bronchial circulation in the injury since blockade of bronchial blood flow will also minimize the pulmonary injury. The data suggest that cytotoxins or activated cells are formed in the airway and carried to the parenchyma. These materials cause the formation of oedema and a reduction of PaO(2).
烧伤患者吸入烟雾是一个全球性的严重医学问题。除了增加感染、呼吸机使用天数和住院时间外，吸入性损伤还会增加死亡率。此外，还有大量未烧伤的患者因烹饪火灾、焚烧作物和森林火灾而吸入烟雾。由于气道阻塞、肺血管跨膜液体通量增加和缺氧性肺血管收缩丧失，这种损伤会导致动脉氧合下降。心肺功能的变化至少部分是由活性氧和氮物质介导的。一氧化氮（NO）由一氧化氮合酶（NOS）的诱导型和组成型同工型产生。NO与超氧化物结合形成活性氮物质，如过氧亚硝酸盐。这些活性氮物质可以通过测量它们的反应产物，如3-硝基酪氨酸来检测。烟雾/烧伤损伤后气道中3-硝基酪氨酸水平会升高。NO生成的控制涉及聚（ADP核糖）聚合酶（PARP）及其通过核糖基化上调核转录因子活性的能力。目前的数据还支持支气管循环在损伤中起主要作用，因为阻断支气管血流也能将肺损伤降至最低。数据表明，细胞毒素或活化细胞在气道中形成并输送到实质组织。这些物质会导致水肿形成和动脉血氧分压（PaO₂）降低。
