心房钠尿肽对急性肺损伤的治疗作用及其可能机制  

Effect of atrial natriuretic peptide on acute lung injury and possible mechanism

作　　者：闫志强[1] 李志超[1] 李志斌[1] 宋景春[1] 魏敏[2] 

机构地区：[1]第四军医大学基础部病理生理学教研室,陕西西安710033 [2]新疆军区喀什军分区卫生所,新疆喀什844200

出　　处：《第四军医大学学报》2004年第23期2199-2201,共3页Journal of the Fourth Military Medical University

摘　　要：目的 :研究心房钠尿肽 (ANP)对急性肺损伤时肺泡Ⅱ型上皮细胞 (AT Ⅱ )的保护作用及其机制 .方法 :SD大鼠18只随机等分为生理盐水对照组、脂多糖 (LPS)模型组、ANP治疗组 .通过颈外静脉给药 ,给药 4h后处死动物 ,收集肺泡灌洗液 (BALF) ,测定BALF表面张力、总磷脂含量 (TPL)、乳酸脱氢酶 (LDH)、碱性磷酸酶 (AKP)、丙二醛 (MDA)及总蛋白 (TP)含量 .结果 :与对照组比较 ,LPS可使BALF中LDH活性 [(4.8± 1.9) ,(8.4± 1.9) μkat/L]及TP含量升高 (P <0 .0 5 ) ,ANP[(5 .1± 1.7) μkat/L]可逆转此现象 ;LPS可使BALF中TPL[(0 .4 3± 0 .0 4 )vs (0 .34± 0 .0 6 ) μg/kg]明显降低 (P <0 .0 5 )、表面张力 [(19.8± 2 .6 )vs (2 3.3± 2 .9)mN/m]升高 (P <0 .0 5 ) ,ANP治疗后TPL[(0 .4 1± 0 .0 6 ) μg/kg]升高、表面张力 [(18.6± 2 .9)mN/m ]降低 ;与对照组比较 ,LPS组AKP活性 [(0 .10± 0 .0 8)vs (0 .36± 0 .10 ) μkat/L]升高 (P <0 .0 5 ) ,ANP治疗后AKP[(0 .14± 0 .0 9) μkat/L]明显降低 ;ANP能逆转LPS引起的MDA含量升高 .结论 :ANP能减轻LPS引起的急性肺损伤 ,其机制可能与ANP保护AT Ⅱ并促进其分泌表面活性物质有关 .AIM: To study the protective effect of atrial natriuretic peptide (ANP) on alveolar typeⅡ cells (AT-Ⅱ) from lipopolysaccharide (LPS) induced acute lung injury (ALI). METHODS: Eighteen rats were divided into 3 groups: Control group were injected physiological saline through jugular, LPS group were injected LPS and physiological saline through jugular and ANP group were injected LPS and ANP through jugular. Four hours later, rats were sacrificed and the bronchoalveolar lavage fluid (BALF) was collected. Surface tension, total phospholipids (TPL), total protein (TP) and maleic dialdehyde (MDA) content of the BALF were measured. The activity of lactate dehydrogenase (LDH) and alkaline phosphatase (AKP) in BALF were detected. RESULTS: Compared with those of control group, LPS can increase the TP content and the activity of LDH [Control Group (4.8±1.9) μkat/L, LPS Group (8.4± 1.9) nkat/L in BALF (P<0 .05), which could be reversed by ANP (5.1±1.7) μkat/L]. TPL [(0.43±0.04) vs (0.34±0.06) μg/kg] increased and surface tension [(19.8±2.6) vs (23.3±2.9) mN/m] decreased in LPS group (P<0.05), but no difference was found between ANP group [TPL (0.41±0.06) μg/kg; surface tension (18.6±2.9) mN/m] and control group. ANP prevented the increase of the AKP activity [Control Group (0.10± 0.08) μkat/L, LPS Group (0.36±0.10) μkat/L, ANP Group (0.14± 0.09 ) μkat/L] and the content of MDA in BALF (P<0.05) induced by LPS. CONCLUSION: ANP can protect the lung from injury by LPS in ALI. One of the most important mechanisms is possibly that ANP can protect the AT-Ⅱ and facilitate the secretion of PS.

关 键 词：心钠素 肺表面活性物质 呼吸窘迫综合症 成人 

分 类 号：R563.1[医药卫生—呼吸系统]