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目的:探讨肾性高血压大鼠心肌组织和血浆血管紧张素Ⅱ(AngⅡ)和醛固酮(Ald)的变化对心肌肥厚和心功能的影响,并观察AngⅡ受体拮抗剂缬沙坦对心肌肥厚和心功能的治疗作用。方法:34只SD大鼠分为缬沙坦治疗组(13只,V组),非缬沙坦治疗组(11只,NV组)和假手术组(10只,S组)。V组和NV组在左肾动脉置入内径为0·3mm的银夹(2K1C)。术后2周,V组每天给予缬沙坦30mg/kg,一次性灌胃治疗;S组和NV组每天给予相同容量的饮用水灌胃,共10周。观察各组大鼠的血压、心脏结构、心肌收缩功能、血浆和心肌中AngⅡ、Ald的变化。结果:①各组间治疗前体重、尾动脉收缩压、左室质量(LVM)、相对室壁厚度(RWT)、左室射血分数(LVEF)、短轴缩短率(FS)、中层短轴缩短率(mFS)、室壁应力(MESS)均差异无统计学意义(均P>0·05);②NV组术后第10周尾动脉收缩压、RWT、LVM、LVM指数(LVMI)较S组和V组均明显增加,而左室舒张末期内径(LVDd)明显减小,差异有统计学意义(均P<0·01)。V组高于S组,但差异无统计学意义(均P>0·05);③NV组的LVEF、MESS、mFS、实测mFS/预测mFS明显小于S组和V组(均P<0·05),V组和S组比较差异无统计学意义(P>0·05);④V组和NV组大鼠血浆AngⅡ明显高于S组(均P<0·01),V组和NV组比较差异无统计学意义(P>0·05);⑤血浆Ald各组比较差异无统计学意义(P>0·05),心肌组织Ald NV组与V组比较差异差异有统计学意义(P<0·05),但与S组比较无统计学意义。结论:①2K1C大鼠可产生明确的肾素增高所致的高血压左室肥厚和心功能不全;②Ald与高血压左室肥厚和几何构型及其心力衰竭发展密切相关;③缬沙坦可抑制左室肥厚和收缩功能不全的发生发展。
Objective: To investigate the effects of angiotensin Ⅱ (Ang Ⅱ) and aldosterone (Ald) on myocardial hypertrophy and cardiac function in renal hypertensive rats and to observe the effect of Angiotensin Ⅱ receptor antagonist valsartan on cardiac hypertrophy and Therapeutic effect of heart function. Methods: Thirty-four SD rats were divided into three groups: Valsartan group (13 rats), Valsartan non-valsartan group (11 rats, NV group) and sham operation group (10 rats). V group and NV group in the left renal artery into the diameter of 0.3 mm silver clip (2K1C). After 2 weeks, group V was given valsartan 30mg / kg every day for one time. Group S and group NV were given the same volume of drinking water daily for 10 weeks. The changes of blood pressure, cardiac structure, myocardial contractile function, Ang Ⅱ, Ald in plasma and myocardium were observed. Results: The body weight, the systolic pressure of the tail artery, left ventricular mass (LVM), relative wall thickness (RWT), left ventricular ejection fraction (LVEF), short axis shortening (FS) There was no significant difference in shortening rate (MFS) and wall stress (MESS) between the two groups (all P> 0.05); ② The systolic pressure, RWT, LVM and LVM index Group V and Group V were significantly increased, while left ventricular end-diastolic diameter (LVDd) was significantly reduced, the difference was statistically significant (P <0.01). VV group was higher than S group, but the difference was not statistically significant (all P> 0.05); ③VVV group LVEF, MESS, mFS, mFS / mFS was significantly lower than the S and V groups (P <0.05 (P 0. 05) .④The plasma levels of AngⅡ in group V and group NV were significantly higher than those in group S (all P <0.01), and those in group V and group NV were significantly lower than those in group S There was no significant difference between the Ald NV group and the V group (P> 0.05); ⑤ There was no significant difference in plasma Ald (P> 0.05) 0.05), but no significant difference with the S group. Conclusion: ①K1C rats can produce a clear increase of renin induced hypertensive left ventricular hypertrophy and cardiac insufficiency; ② Ald and hypertensive left ventricular hypertrophy and geometry and its development of heart failure are closely related; ③ valsartan can inhibit Left ventricular hypertrophy and systolic dysfunction occurred.