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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。
AIM: To investigate the effect of Nicorandil, an ATP-sensitive potassium channel opener, on pulmonary vascular remodeling in monocrotaline-induced pulmonary hypertension in mice. Methods: CD1 male mice were randomly divided into control group, monocrotaline model group and monocrotaline plus nicorandil group, with 6 mice in each group. Subcutaneous injection of monocrotaline (400 mg / kg) The model of pulmonary hypertension was established once a week for 8 weeks. The treatment group was administered with nicorandil (10.5 mg / kg) daily. Right ventricular systolic pressure was measured by right ventricular puncture method directly after 8 weeks. Right ventricular hypertrophy index was calculated by weighing method. Morphology of right ventricular myocardium was observed by HE staining. Median thickness of pulmonary arterioles was measured by elastic fiber staining. Expression of α-smooth muscle actin (α-SMA) in pulmonary artery smooth muscle cells and calculate the degree of pulmonary arterialization. RESULTS: Nicorandil (10.5 mg / kg) significantly reduced monocrotaline-induced right ventricular systolic pressure (P <0.01) and right ventricular hypertrophy (P <0.05) Thick (P <0.01), inhibit the complete remodeling of pulmonary arterioles (P <0.01) and alleviate the damage of right ventricular myocytes. CONCLUSION: Nicorandil attenuates monocrotaline-induced pulmonary hypertension by inhibiting pulmonary vascular remodeling, which may be a drug that can effectively prevent and treat pulmonary hypertension.