硫化氢对大鼠肺的损伤作用

Pulmonary Injury due to Hydrogen Sulfide Inhalation in Rats

Wistar大鼠见入不同浓度硫化氢(0、100、200ppm)3h后不同时间收集支气管肺泡灌洗液(BALF)进行分析,观察硫化氢(H_2S)对肺的损伤作用,发现H_2S吸入后导致BALF中乳酸脱氢酶(LDH)、碱性磷酸酶(AKP)、酸性磷酸酶(ACP)、细胞总数(TC)、中性多形核白细胞(PMN)、唾液酸(SA)、蛋白以及血管紧张素转换酶(ACE)、磷脂(PL)含量明显增高。增高的峰值一般多在吸入后1h或6h,少数指标为12h。增高的程度与恢复时间均与吸入H_2S的浓度有关。实验结果表明H_2S对肺有强烈的细胞毒作用。磷脂含量的变化提示肺泡表面活性物质受损;ACE活性变化与SA及蛋白含量呈高度相关(前者r=0.86,P<0.01;后者r=0.87,P<0.01),说明肺血管通透性增加导致的肺水肿与血管内皮细胞受损有关。同时,肺泡表面活性物质受损也参与H_2S中毒性肺水肿的形成。这些结果与光、电镜观察相一致。

Witsar rats were forced to inhale air containing 0 , 100, and 200ppm of hydrogen sulfide (H2S) for 3 hours, and the brocho-alveolar lavagefluid (BALF) of the rats was collected and analyzed in different period afterinhalation to observe the pulmonary injury H2S produced. It was found thatH2S inhalation resulted in an increase of the content of lactate dehydrogenase,alkaline phosphatase, acid phosphatase, total number of cells, polymorphonu-clear leucocytes, sialic acid, protein, angiotensin converting enzyme, and pho-spholipid in BALF. Peak elevation of most parameters occurred in the 1st or6th hour after inhalation, but a few of them in the 12th hour. The extent ofelevation and the rapidity of recovery of the parameters were dependent on theamount of H2S inhaled.It is concluded that H2S inhalation can exert severe cytotoxic and edema-togenic effects on the pulmonary parenchyma,Changes of phospholipid in BALF suggests the damage on alveolar surfactants. Changes of angiotensin converting enzyme level were correlated with those of protein and saliac acid in BALF of the intoxicated rats (r = 0.86, P<0.01 and r = 0.87, P<0.01 respectively) , which indicates that pulmonary edema resulting from increased vascular permeability is closely related to the injury of pulmonary vascular epithelium. Moreover, the injury of alveolar surfactants also plays a part in the development pulmonary edema. These findings are in agreement with the pathological findings of the intoxicated rats.