文章摘要
邵成杰,孔 辉,曾晓宁,李 湘,朱家丽,解卫平,王 虹.尼可地尔抑制野百合碱诱导的肺动脉高压小鼠肺血管重构[J].南京医科大学学报,2017,(8):943~948
尼可地尔抑制野百合碱诱导的肺动脉高压小鼠肺血管重构
Nicorandil alleviates monocrotaline-induced pulmonary artery hypertension by inhibiting pulmonary vascular remodeling
投稿时间:2017-02-23  
DOI:10.7655/NYDXBNS20170805
中文关键词: 肺动脉高压  ATP敏感性钾离子通道  尼可地尔  野百合碱
英文关键词: pulmonary artery hypertension  adenosine triphosphate-sensitive potassium channel  nicorandil  monocrotaline
基金项目:国家自然科学基金(81273571)
作者单位
邵成杰 南京医科大学第一附属医院呼吸与危重症学科江苏 南京 210029 
孔 辉 南京医科大学第一附属医院呼吸与危重症学科江苏 南京 210029 
曾晓宁 南京医科大学第一附属医院呼吸与危重症学科江苏 南京 210029 
李 湘 南京医科大学第一附属医院呼吸与危重症学科江苏 南京 210029 
朱家丽 南京医科大学第一附属医院呼吸与危重症学科江苏 南京 210029 
解卫平 南京医科大学第一附属医院呼吸与危重症学科江苏 南京 210029 
王 虹 南京医科大学第一附属医院呼吸与危重症学科江苏 南京 210029 
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中文摘要:
      目的:研究ATP敏感性钾离子通道开放剂尼可地尔对野百合碱诱导的肺动脉高压小鼠肺血管重构的影响。方法:CD1雄性小鼠随机分为对照组、野百合碱模型组、野百合碱+尼可地尔治疗组,每组6只,后2组给予野百合碱(400 mg/kg)皮下注射,每周1次,连续8周,制备肺动脉高压模型,治疗组每日给予尼可地尔(10.5 mg/kg)灌胃。8周后通过直接经膈肌右心室穿刺法测定右心室收缩压;称重法计算右心肥厚指数;HE染色观察右室心肌细胞形态;弹力纤维染色测定肺小动脉中膜厚度;免疫组化检测肺动脉平滑肌细胞α-肌动蛋白(α-smooth muscle actin,α-SMA)表达并计算肺小动脉肌化程度。结果:尼可地尔(10.5 mg/kg)能显著降低野百合碱诱导的小鼠右心室收缩压升高(P<0.01)和右心肥厚(P<0.05),减轻肺小动脉中膜增厚(P<0.01),抑制肺小动脉完全肌化(P<0.01),减轻右心心肌细胞损伤。结论:尼可地尔能通过抑制肺血管重构减轻野百合碱诱导的肺动脉高压,其可能是一种能有效防治肺动脉高压的药物。
英文摘要:
      Objective: To investigate the effect of nicorandil, an adenosine triphosphate-sensitive potassium channel opener, on pulmonary vascular remodeling in monocrotaline-induced mice model of pulmonary artery hypertension. Methods: CD1 male mice were randomly divided into control group, monocrotaline group, and monocrotaline+nicorandil group(n=6 for each group). The latter 2 groups were subcutaneously injected with 400 mg/kg monocrotaline weekly for 8 weeks to induce pulmonary artery hypertension model. The mice in the monocrotaline+nicorandil group were treated with 10.5 mg/kg nicorandil daily by intragastric administration. After 8 weeks, the right ventricular systolic pressure was evaluated by right ventricular puncture through the diaphragm; the index of right ventricular hypertrophy was calculated; the morphologic changes of right ventricle cardialmyocytes were detected by HE staining; the thickness of pulmonary arterial media wall was measured by elastin staining; α-smooth muscle actin (α-SMA) immunohistochemitry was used to assay pulmonary arterioles muscularization. Results: Daily treated with nicorandil (10.5 mg/kg) for 8 weeks significantly decreased RVSP (P<0.01), attenuated the index of right ventricular hypertrophy (P<0.05), alleviated the thickness of pulmonary arterial media wall (P<0.01), declined the ratio of fully-muscularized pulmonary arterioles (P<0.01), and prevented the injury of right ventricle cardialmyocytes. Conclusion: Nicorandil could relieve monocrotaline-induced pulmonary artery hypertension by inhibiting pulmonary vascular remodeling. It could be a potential drug for preventing and treating pulmonary artery hypertension.
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