小剂量安体舒通抗左旋硝基精氨酸诱导持续性高血压大鼠心肌纤维化  

The effects of spironolactone on hypertensive myocardial fibrotic rats induced by NomeganitroLarginine(LNNA)

作　　者：谢晓华[1] 王士雯[1] 叶平[1] 马卫东 卢丽华[1] 唐朝枢[1] 

机构地区：[1]解放军总医院老年心血管病研究所

出　　处：《军医进修学院学报》1998年第1期26-28,共3页Academic Journal of Pla Postgraduate Medical School

摘　　要：目的：探讨小剂量醛固酮受体拮抗剂安体舒通抗左旋硝基精氨酸（ＬＮＮＡ）诱导高血压心肌纤维化的可行性。方法：复制ＬＮＮＡ诱导持续性高血压心肌纤维化大鼠模型２５只，以小剂量安体舒通２０ｍｇ／（ｋｇ·ｄ）处理后与对照组对比观察。结果：动脉血压及血浆ＮＯ－２浓度可自然逆转，但心肌组织胶原蛋白含量、心脏相对重量均无显著逆转。小剂量安体舒通治疗可明显降低胶原蛋白含量、心脏相对重量及ＡⅡ水平。结论：一氧化氮生成减少，导致醛固酮与心肌组织醛固酮受体结合增加，并介导ＬＮＮＡ诱导持续性高血压大鼠心肌纤维化。小剂量安体舒通通过竞争性抑制醛固酮与其受体结合，可逆转心肌纤维化。Objective:The present study was designed to detect antifibrotic effects of low dose aldosterone(ALDO) receptor anatagonistspironolactone (spiron) on the sustained hypertensive myocardial fibrosis induced by LNNA. Methods:The plasma and myocardial angiotensin Ⅱ(AⅡ) and ALDO, serum NO-2 and left ventrical myocardial collagen content (C) were determined in the untreated and treated 18 rat models of hypertensive myocardial fibrosis with spiron (20 mg/kg,1/d, by gavage)and in control (7 wistar rats). Results:(1)The natural regressive effects were found in serum NO-2(P<0.05) and arterial blood pressure (ABP) (P<0.01). But the natural regression in heartbody weight ratio (HWR) and C werent found. (2)The spiron treatment abolished the significant increases in the levels of HWR, AⅡ, but didnt affact ABP and the level of serum NO-2.Conclusion:These data suggest that the development of myocardial fibrosis in this model may be related to the increase in the density of ALDO binding with its receptors mediated by the decrease of NO synthesis, and the low dose spiron treatment may make the myocardial fibrosis regress, possibly via its competitive inhibiting action at ALDO binding with its receptors.

关 键 词：安体舒通 剂量 高血压 心肌纤维化 

分 类 号：R542.2[医药卫生—心血管疾病] R544.105[医药卫生—内科学]