摘要
刺激性气体引起的化学性肺损伤与一氧化碳中毒是烟雾吸入伤的重要致病因素。本实验比较酸吸入犬(对照组)与迭加一氧化碳中毒犬(实验组)血液动力学与氧代谢的改变。结果表明,单纯酸吸入及合并一氧化碳中毒均导致血压与心输出的下降。实验犬PaO_2明显低于对照犬。碳氧血红蛋白增高使实验组氧转运下降,尽管氧提取率代偿增高,但氧耗量与PVO_2明显降低。提示一氧化碳吸入加剧了酸吸入时机体的氧代谢障碍。
Chemical pneumonitis and carbon monoxide (CO) poisoning may be the etiologic factors in inhalation injury. Since the CO poisoning related with smoke inhalation has a much high mortality we tested the hypothesis that superimposed CO poisoning deteriotes hemodynamics and oxygen metabolism in acid inhalation injury. Ten anesthetized dogs were ventilated in room air to maintain normal PaCO2. Lung injury was produced with 2ml/kg 0.1 N HCL intratracheally. Five dogs (ACID) were then ventilated with room air, while the others were exposed to 1%CO in air for 10 minutes to produce CO poisoning simultanueously with acid instillation (Co-ACID). Hemodynamic changes, oxygen metabolism and carboxyhe- moglobin (COHb) were monitored for 4 hours. Thirty minutes following the challenge PaO2 in ACID and CO-ACID groups fell to 65±10 and 43±4 (p<0.05), respectively. Acid caused significantly decreased cardiac output and inereased pulmonary vascular resistance. CO did not accentuate hemodynamic changes following acid inhalation. However, a signifi- cant increase of COHb in CO-ACID group resulted in deterioration of oxygen transporta- tion. Though oxygen extraction increased markedly in both groups the oxygen consumption decreased significantly in CO-ACID group. A constantly depressed mixed venous oxygen tension in CO-ACID group suggests the deterioration of tissue oxygen metabolism.
