论文部分内容阅读
本文观察了自由基机制在大鼠硫化氢吸入中毒肺损伤中的作用。测定了肺组织及支气管肺泡灌洗液中丙二醛(MDA)、灌洗液蛋白浓度和细胞学变化;肺及血液SOD、GSH和Vit E。结果表明,大鼠在吸入H_2S后,MDA显著增加,灌洗液蛋白浓度明显增加,细胞学变化提示炎症反应明显。SOD活性先抑制后增强,GSH和Vit E在中毒后显著降低。上述各项指标变化的严重程度与硫化氢的吸入浓度有关。浓度高,损伤重,变化早,恢复慢。H_2S中毒导致自由基形成和脂质过氧化的增强是H_2S所致肺损伤的机制之一,其损伤程度与剂量有关。
This article observed the role of free radical mechanisms in lung injury induced by hydrogen sulfide inhalation in rats. The contents of malondialdehyde (MDA), lavage fluid and cytology in lung tissue and bronchoalveolar lavage fluid were measured. The SOD, GSH and VitE in lung and blood were measured. The results showed that after inhaled H2S, the MDA increased significantly and the protein concentration in lavage fluid increased obviously. The cytological changes suggested that the inflammatory reaction was obvious. SOD activity was inhibited first increased, GSH and Vit E significantly reduced after poisoning. The above indicators of the severity of changes and the concentration of hydrogen sulfide inhalation. High concentrations, heavy damage, changes early, slow recovery. H 2 S poisoning leads to the formation of free radicals and lipid peroxidation enhancement is one of the mechanisms of H 2 S-induced lung injury, the degree of damage and dosage.