脑血管病并发神经源性肺水肿炎症机制的探讨

Nvestigation on the Inflammatory Mechanism of Cerebral Vascular Disease Complicated With Neurogenic Pul- monary Edema

目的:讨脑血管病(CVD)并发神经源性肺水肿(NPE)的炎症反应机制。方法:选择(CVD)患者65例和健康体检者24例;血清内皮素(ET-1)测定方法采用人ET-1酶免疫检测试剂盒;血清TNF-α测定采用双夹心ELISA法;血清超敏C反应蛋白(hsCRP)水平测定采用免疫比浊法。结果:(CVD)组ET-1、TNF-α、hsCRP水平均高于对照组(P<0.05);并发NPE的患者ET-1、TNF-α水平均高于无NPE的患者(P<0.05)。结论:ET-1和TNF-α介导的炎症损伤机制在神经源性肺水肿中可能起重要作用。

Objective： To explore the inflammatory mechanism of cerebral vascular disease （ CVD） complicated with neurogenic pulmonary edema （ NPE） . Methods： Sixty-five cases with CVD and 26 healthy volunteers were involved in the study. Endothelin-1 （ ET-1） was detected by the human TiterZyme Enzyme Immunometric Assay （ EIA） Kit,plasma level of tumor necrosis factor （ TNF-a） was measured by the method of ELISA and the serum level of high sensitivity C-reactive protein （ hsCRP） was measured with immune turbidimetry. Results： Levels of ET-1,TNF-α and hsCRP were higher in patients with CVD than those in the healthy controls （ P 0. 05） ; and the levels of ET-1,TNF-α and hsCRP in patients complicated with NPE were higher than those without NPE （ P 0. 05） . Conclusion： The mechanism of inflammatory injury induced by ET-1 and TNF-α may play an important role in NPE.