摘要
目的 观察丹参防治左室肥厚的作用机制。方法 用自发性高血压大鼠为心肌肥厚模型 ,18只 8周龄的自发性高血压大鼠随机分成三组 :一组于 8周时处死 ,另两组分别经腹腔注射丹参或蒸馏水[(1ml/ (kg·d) ]10周。测量大鼠尾动脉收缩压 (SBP)及左心室重量指数 (LVMI)。检测大鼠心肌组织中去甲肾上腺素 (NE)、多巴胺 (DA)、肾上腺素 (E)及超氧化物歧化酶 (SOD)、谷胱甘肽过氧化物酶(GSH Px)、过氧化脂质 (LPO)、血管紧张素 Ⅱ (AngⅡ )的含量。结果 ①丹参组大鼠SBP及LVMI指标与高血压组比较均明显降低 ;②丹参可抑制NE、DA含量的降低和E含量的增高 ;③丹参可增强心肌组织SOD和GSH Px 活性 ,减少LPO的生成 ;④丹参可降低左心室肥厚组织Ang Ⅱ含量的增高。结论 丹参能有效防治自发性高血压大鼠左室肥厚的发生。它作用机制与丹参调整和改善心脏局部儿茶酚胺、氧自由基代谢有关 ,而且还与丹参抑制体内肾素 -血管紧张素系统 (RAS)代谢相关。
Objective To observe the effects of radix salviae miltiorrhizae(RSM) on left ventricular hypertrophy (LVH) model in spontaneously hypertensive rats (SHRs),and investigate its mechanisms.Methods 18 8-week-old SHRs were divided into three groups at random.The rats in group one were killed at 8 weeks.RSM or distilled water[1mg/(kg·d)]was injected through intraperitoneally for 10 weeks. Systolic blood pressure (SBP) and left ventricular mass index(LVMI)were measured.The norepinephrine (NE),dopamine(DA),adnephrin(E) and superoxide dismutase(SOD),glutathione peroxidase(GSH-Px),lactoperoxidase(LPO),angiotensin Ⅱ (Ang Ⅱ) expression in the left ventricular tissue of SHRs were measured.Results ① Compared with hypertension group, the SBP and LVMI were significantly lower after using RSM.② RSM more effectively prevented the depletion of NE, DA and elevation of E produce in myocardial than distilled water.③RSM promoted the SOD,GSH-Px activities and decreased LPO produce in myocardia.④RSM significantly prevented the increase of Ang Ⅱ content in LVH tissue.Conclusion RSM may effectively prevent and treat the LVH of SHRs.The effect of RSM on anti-hypertrophy is associated with regulating and improving the metabolism of catecholamine and oxygen-derived,free radicals in the heart,and is closely associated with inhibiting the metabolism of RAS.
出处
《中华急诊医学杂志》
CAS
CSCD
2004年第5期322-324,共3页
Chinese Journal of Emergency Medicine
基金
湖北省自然科学基金资助项目 ( 2 0 0 0J0 64 )
关键词
丹参
自发性高血压
大鼠
左室肥厚
预防
治疗
并发症
Spontaneously hypertension
Left ventricular hypertrophy (LVH)
Radix salviae miltiorrhizae(RSM)
Catecholamine (CA)
Oxygen-derived free radicals