摘要
目的:制备离体人肺脏模型,探讨β3肾上腺素能受体激动剂CGP-12177对肺泡液体清除率(AFC)的作用及其机制。方法:以肺泡内Evans蓝标记的白蛋白浓度的变化测定AFC。首先将10-4 mol/L到10-7 mol/L的CGP-12177分别灌注到离体人肺脏肺泡腔内,测定AFC的变化。然后将10-5 mol/L CGP-12177分别与α受体阻滞剂酚妥拉明、β1受体阻滞剂阿替洛尔、β2受体阻滞剂ICI-118551、β3受体阻滞剂SR59230A、钠通道阻断剂氨氯吡咪、Na+-K+-ATP酶阻断剂哇巴因混合后灌注到离体人肺脏肺泡腔内,测定AFC的变化。结果:10-7 mol/L和10-4 mol/L CGP-12177对离体人肺脏肺泡液体清除率没有影响,10-6 mol/L和10-5 mol/L的CGP-12177能够显著提高离体人肺脏肺泡液体清除率。CGP-12177增加离体人肺脏AFC的作用能够被SR59230A、氨氯吡咪和哇巴因抑制。结论:高选择性CGP-12177主要通过调节Na+-K+-ATP酶的活性提高离体人肺脏肺泡液体清除能力。
AIM：To establish the model of isolated human lung,and to study the effect of CGP-12177on alveolar fluid clearance（AFC）in isolated human lung and the mechanisms involved.METHODS：The AFC was measured by the concentration of Evansblue-labeled album in the istilled and aspirated solution.Isomolar albumin solution in the presence of 10^-4 mol/L to 10^-7 mol/L CGP-12177（selectiveβ3-adrenergic agonists）was injected into the alveolar spaces in isolated human lung,and AFC was measured.10-5 mol/L CGP-12177combined with phentolamine（αreceptor antagonist）,atenolol（β1receptor antagonist）,ICI-118551（β2receptor antagonist）,SR59230A（β3receptor antagonist）,sodium channel blockers or Na^＋/K^＋-ATPase blockers were perfused into the alveolar space of isolated human lung.RESULTS：10^-5 mol/L and 10^-6 mol/L CGP-12177increased AFC significantly in isolated human lung,but 10-^4 mol/L and 10^-7 mol/L CGP-12177didn＇t increase AFC.The AFC-stimulating effect of CGP-12177 was decreased by SR59230A,amiloride and ouabain.CONCLUSION：CGP-12177,aβ3-adrenergic agonist,can increase AFC in isolated human lung by promoting the transport of Na^＋-K^＋-ATPase.
出处
《中国临床药理学与治疗学》
CAS
CSCD
2014年第3期271-274,共4页
Chinese Journal of Clinical Pharmacology and Therapeutics
基金
辽宁省科学技术计划项目(201202245)
教育部留学回国人员科研启动基金(教外司留[2011]1139)
