[1]张群燕,蔡 辉,董晓蕾,等.卡托普利对实验大鼠左室肥厚的干预作用[J].医学研究与战创伤救治(原医学研究生学报),2010,12(01):6-8.
ZHANG Qun-yan,CAI Hui,DONG Xiao-lei,et al.Regressing left ventricular hypertrophy by captopril in rat with pressure overload[J].JOURNAL OF MEDICALRESEARCH —COMBAT TRAUMA CARE,2010,12(01):6-8.
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卡托普利对实验大鼠左室肥厚的干预作用(
)
ZHANG Qun-yan,CAI Hui,DONG Xiao-lei,et al.Regressing left ventricular hypertrophy by captopril in rat with pressure overload[J].JOURNAL OF MEDICALRESEARCH —COMBAT TRAUMA CARE,2010,12(01):6-8.
)《医学研究与战创伤救治》（原医学研究生学报）[ISSN:1672-271X/CN:32-1713/R]
- 卷:
- 第12卷
- 期数:
- 2010年01期
- 页码:
- 6-8
- 栏目:
- 出版日期:
- 2010-01-20
文章信息/Info
- Title:
- Regressing left ventricular hypertrophy by captopril in rat with pressure overload
- 文章编号:
- 1672-271X(2010)01-0006-03
- 分类号:
- R541
- DOI:
- -
- 文献标志码:
- A
- 摘要:
- 目的 观察卡托普利逆转压力负荷增加大鼠左室肥厚的作用。方法 采用腹主动脉狭窄所致压力负荷增加大鼠左室肥厚模型，将雄性SD大鼠36只随机分为假手术组、模型组、卡托普利组，观察用药4周后左室重量指数(LVMI)、左室心肌病理形态HE染色、左室心肌细胞超微结构等指标的改变。结果 模型组LVMI明显高于假手术组(P<0.01)，卡托普利组(2.32±0.35)明显低于模型组(2.98±0.36)，P<0.01；左室心肌病理形态HE染色、左室心肌细胞超微结构的改变与LVMI的改变基本一致。结论 卡托普利具有逆转心肌肥厚的作用。
- Abstract:
- Objective To observe the effects of captopril on regressing left ventricular hypertrophy in rat with pressure overload. Methods The model of left ventricular hypertrophy in rat with pressure overload by abdominal aortic constriction was used.36 SD male rats were randomly divided into 3 groups: sham operation group, model group and captopril group. After treatment 4 weeks, it was observed that the changes of myocardial hypertrophy [left ventricular mass index (LVMI), left ventricular myocardium HE staining, left ventricular myocytes ultramicrostructure]. Results LVMI in model group(2.32±0.35) was increased significantly than that in sham operation group (P＜0.01). LVMI in captopril group was lower than that in model group (2.98±0.36)(P＜0.01). The changes of left ventricular myocardium HE staining and left ventricular myocytes ultramicrostructure were consistent with those of LVMI. Conclusion Captopril had the effect on regressing left ventricular hypertrophy.
参考文献/References:
[1] Rosei EA, Muiesan ML, Salvetti M, et al. Evaluation of subclinical target organ damage for risk assessment and treatment in the hypertensive patients: left ventricular hypertrophy [J]. J Am Soc Nephrol, 2006, 17 (4 Suppl 2): S104-S108.
[2] Doering CW, Jalil JE, Janicki JS, et al. Collagen network remodelling and diastolic stiffness of the rat left ventricle with pressure overload hypertrophy[J]. Cardiovasc Res, 1998, 22(5): 686-695.
[3] Simone GD, Kizer JR, Chinali M, et al. Normalization for body size and population-attributable risk of left ventricular hypertrophy: the strong heart study [J]. AJH, 2005, 18 (2 Pt 1):191-196.
[4] Stansfield WE, Rojas M, Corn D, et al. Characterization of a model to independently study regression of ventricular hypertrophy [J]. J Surg Res, 2007, 142(2): 387-393.
[5] Gradman AH, Alfayoumi F. From left ventricular hypertrophy to congestive heart failure: management of hypertension heart disease [J]. Progr Cardiovasc Dis, 2006, 8(5): 326-341.
[6] Li J, Doerffel Y, Hocher B, et al. Inflammation in the genesis of hypertension and its complications-the role of angiotensin Ⅱ [J]. Nephrol Dial Transplant, 2007, 22(11): 3107-3109.
[7] 李昌繁, 江时森. 心力衰竭动物模型的研究进展[J].医学研究生学报, 2007, 20(5):532-534.
[8] Brooks WW, Conrad CH, Robinson KG, et al. L-arginine fails to prevent ventricular remodeling and heart failure in the spontaneously hypertensive rat[J]. Am J Hypertens, 2009, 22(2): 228-234.
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- 备注/Memo:
- 南京军区南京总医院科研基金资助项目(Q2008042)
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