卡托普利长程干预对自发性高血压大鼠左心室重塑及冠脉微血管结构的影响

Effects of long-term administration of captopril onleft ven tricular hypertrophy structure of coronary microcirculation in spontaneous hypert ensive rats

目的 :以自发性高血压大鼠 (SHR)为研究对象 ,观察血管紧张素转换酶抑制剂 (ACEI)卡托普利对SHR左室肥厚、左室心肌纤维化及冠脉微血管结构的影响。方法 :2 0周龄雄性SHR 2 0只 ,随机分为卡托普利(Cap)干预组和对照组 ,每组 10只 ,观察卡托普利干预后 13周内血压变化 ,并于观察期末测左心室重 /体重 (LVW /BW ) ;通过图像分析、形态学观察 ,确定左心室胶原分数 (CF)、标准化血管周胶原面积 (PVCA)及肌间动脉中膜厚度(AMT)。结果 :卡托普利 ( 10 0mg·kg-1·d-1)可使SHR的SBP显著降低 ,治疗 4周后达最大降压效应 ,且该效应于第 13周末仍可维持 (P <0 0 1) ;Cap干预组LVW /BW显著低于对照组 [( 3 42± 0 2 1)mg/gvs ( 3 96± 0 18)mg/g(P <0 0 1) ] ,CVF、PVCA和AMT在Cap干预组显著亦低于对照组 ,肌间和血管外胶原纤维明显减少 ,动脉中膜变薄。结论 :卡托普利能显著逆转SHR病理性LVH、心肌纤维化及冠脉微血管结构异常 。

Objective To explore the effects of lo ng-term treatment of angiotensin converting enzyme inhibitor (ACEI) captopril o n left ventricular hypertrophy (LVH), cardiac interstitial fibrosis and the chang es of the structure of coronary microcirculation in spontaneous hypertensive rat s (SHR). Methods Twenty male SHR of 20 weeks old were fall into two group randomly, 10 were given captopril, 100 mg·kg -1 ·d -1 by gavage for 4 weeks (Cap group) and another 10 were untreated control. Systoli c blood pressure were measured every week. At the end of 13 weeks, rats were wei ghted and killed. Heart weight (HW), left ventricular weight (LVW) and LVW to bo dy weight ratio (LVW/BW) were determined. The collagen volume fraction (CF), sta ndardized perivascular collagen area (PVCA) and average medial thickness (AMT) o f intramyocardial arterial in left ventriclar myocardial were measured by autom atic image analyzer. Results Compared with control group, th e systolic blood pressure decreased significantly in Cap group, which reached to the most extent level at 4 th week [(18.6±0.52) kPa vs (25.6±0.92) k Pa (P<0.01)], and maintained at this lower level till 13th week [(18.1± 0.27) kPa vs (25.0±1.95) kPa, (P<0.01)]. LVW/BW, CVF, PVCA, AMT an d myocardial fibrosis also reduced significantly in Cap group. Conclusi on Long-term treatment of captopril could markedly reverse LVH, myoca r dial fibrosis and abnormalities of coronary microciculation structure and show b enefit effect in cardiac protection.