摘要
目的研究左旋精氨酸(L-Arg)对肺血栓栓塞症的作用及其可能的机制。方法W istar大鼠72只,随机分为对照组、模型组、L-Arg组各24只。采用自体血栓回输的方法制备肺血栓栓塞症模型,模型制备成功后,L-Arg组经腹腔注射L-Arg 100 mg.kg-1。各组于栓塞后1 h、1,3,7 d分别处死,检测动脉血气分析、肺部的形态学变化、血清中一氧化氮(NO)水平,用免疫组化的方法检测肺组织中内皮素(ET-1)蛋白表达。结果模型组肺栓塞后病理检查可见肺动脉血栓形成,炎性反应明显,血清中NO水平下降(P<0.01),而ET-1蛋白表达增加(P<0.01)。L-Arg组肺部病变程度减轻,栓塞1 d后NO水平升高,ET-1蛋白表达下调(P<0.05)。结论L-Arg通过上调NO水平,抑制ET-1的表达,阻止肺血栓栓塞症的进一步发展。
Objective To study the effects of L-arginine （L-Arg） on pulmonary thromboembolism （PTE） and its possible mechanism. Methods Seventy-two rats were randomly divided equally into control group, model group, and treatment group. PTE model was established by intravenous injection of auto-blood clots. In treatment group, L-Arg 100 mg·kg^-1 was injected into peritoneum after model preparation. All rats were sacrificed on 1 hour, 1, 3 and 7 days after pulmonary thromboembolism, respectively. Arterial blood gas analysis and the level of nitric oxide were measured. The changes in lung morphology were observed by microscopy. Endothelin-1 was assessed by immunohistochemical technique and HMIAS image analysis. Results Thrombi in pulmonary arteries and prominent inflammatory reactions were found by microscopy in model group. The level of NO was significantly decreased, while ET-1 expressions were significantly increased in model group （P 〈 0.01）. After administration of L-Arg, the pathological lesions in lung were relieved with NO level higher than that of the model group, and ET-1 expression lower than that of the model group on 1, 3 and 7 days. Conclusion L-Arg may prevent the progress of PTE by increasing NO level and inhibiting expression of ET-1.
出处
《医药导报》
CAS
2006年第9期871-873,共3页
Herald of Medicine
