中国组织工程研究

• 心脏及血管损伤动物模型 Animal models of heart and vascular damage • 上一篇    下一篇

肺高血流模型大鼠肺动脉重构与奈必洛尔的影响

陈 鹏1,江 平1,朱灿阳1,杨 梅1,马洪骏2,黎燕峰1   

  1. 河北医科大学,1基础医学院药理学教研室,2电镜室,河北省石家庄市 050017
  • 出版日期:2015-11-30 发布日期:2015-11-30
  • 通讯作者: 黎燕峰,教授,硕士生导师,河北医科大学基础医学院药理学教研室,河北省石家庄市 050017
  • 作者简介:陈鹏,女,1978年生,山东省庆云县人,汉族,2013年河北医科大学毕业,硕士,主管护师,主要从事临床药理学及护理学研究。
  • 基金资助:

    河北省科学技术研究与发展计划项目(10276105D-11)

Effect of nebivolol on pulmonary artery remodeling in rats with high pulmonary blood flow

Chen Peng1, Jiang Ping1, Zhu Can-yang1,Yang Mei1, Ma Hong-jun2, Li Yan-feng1   

  1. 1Department of Pharmacology, Basic Medical College of Hebei Medical University; 2Electron Microscopy Room, Hebei Medical University, Shijiazhuang 050017, Hebei Province, China
  • Online:2015-11-30 Published:2015-11-30
  • Contact: Li Yan-feng, Professor, Master’s supervisor, Department of Pharmacology, Basic Medical College of Hebei Medical University, Shijiazhuang 050017, Hebei Province, China
  • About author:Chen Peng, Master, Nurse-in-charge, Department of Pharmacology, Basic Medical College of Hebei Medical University, Shijiazhuang 050017, Hebei Province, China
  • Supported by:

    The Science and Technology Research and Development Plan Project of Hebei Province of China, No. 10276105D-11

摘要:

背景:血管舒张型肾上腺素β1受体阻断药奈必洛尔能否有效降低肺动脉压,对肺血管重构有何影响,目前尚不清楚。
目的:观察奈比洛尔对肺高血流模型大鼠肺动脉重构的影响。
方法:将40只SD大鼠随机均分为4组,模型组、奈比洛尔组、卡托普利组均制备肺动脉高压并肺血管重构大鼠模型,假手术组仅分离腹主动脉及下腔动脉;造模后5 d,奈比洛尔组、卡托普利组分别于灌胃给予奈比洛尔溶液1 mg/(kg•d)与卡托普利溶液5 mg/(kg•d),模型组与假手术组灌胃给予等体积生理盐水。给药8周后,对比4组平均肺动脉压、右心室肥厚指数、肺动脉形态学变化、肺动脉超微结构及肺动脉环舒张率。
结果与结论:与假手术组比较,模型组大鼠肺间小动脉肌化  程度明显,平均肺动脉压和右心室湿质量/(左心室湿质量+室间隔湿质量)显著增高(P < 0.01或P < 0.05),肺动脉环舒张率降低(P < 0.05或P < 0.01)。与模型组比较,奈必洛尔组、卡托普利组平均肺动脉压、右心室湿质量/(左心室湿质量+室间隔湿质量)显著降低   (P < 0.05或P < 0.01),肺间小动脉肌化程度降低,肺动脉环舒张率增加(P < 0.05或P < 0.01)。说明奈比洛尔能够减轻肺高血流模型大鼠的肺动脉重构,其机制与奈必洛尔保护血管内皮和降低肺动脉压有关。 

 

关键词: 实验动物模型, 心肺及血管损伤动物模型, 奈比洛尔, 腹主动脉-下腔静脉分流, 肺动脉高压, 血管重构, 血管内皮, 大鼠

Abstract:

BACKGROUND: It is still unclear whether nebivolol, a vasodilatory-type adrenergic β1 receptor antagonist, can effectively reduce pulmonary artery pressure and what is the effect on pulmonary vascular remodeling.
OBJECTIVE: To investigate the effect of nebivolol on pulmonary artery remodeling of rats with high pulmonary blood flow.
METHODS: Forty Sprague-Dawley rats were randomly divided into four groups: model, nebivolol, captopril and sham groups. Rats in the model, nebivolol and captopril groups were prepared to establish rat models of pulmonary hypertension and pulmonary vascular remodeling. Rats in the sham group were only subjected to separation of the abdominal aorta and inferior vena artery. After 5 days of modeling, the rats in the nebivolol group and captopril group were respectively intragastrically administered 1 mg/kg nebivolol solution and 5 mg/kg captopril solution daily. Rats in the model and sham groups were intragastrically administered the same amount of normal saline. After 8 weeks of administration, mean pulmonary arterial pressure, right ventricular hypertrophy index, pulmonary artery morphological changes, pulmonary artery ultrastructure and pulmonary arterial ring diastolic rate were compared among these four groups.
RESULTS AND CONCLUSION: Compared with the sham group, the muscularization of pulmonary arterioles of 
rats in the model group was obvious; mean pulmonary artery pressure and right ventricular wet weight/(left ventricle wet weight+interventricular septum wet weight) were significantly increased (P < 0.05 or P < 0.01); pulmonary arterial ring diastolic rate was decreased (P < 0.05 or P < 0.01). Compared with the model group, mean pulmonary artery pressure and right ventricular wet weight/(left ventricle wet weight + interventricular septum wet weight) were significantly decreased (P < 0.05 or P < 0.01); the muscularization of pulmonary arterioles was alleviated and pulmonary arterial ring diastolic rate was increased in the nebivolol and captopril groups (P < 0.05 or P < 0.01). These results demonstrate that nebivolol can effectively alleviate pulmonary artery reconstruction in rats with high pulmonary blood flow through protecting vascular endothelium and reducing pulmonary artery pressure.  

 

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