左旋精氨酸和维生素C合用对自发性高血压大鼠左室肥厚及血管内皮功能的影响

Effect of L-Arginine and vitamin C on left ventricular hypertrophy and endothelial function in spontaneously hypertensive rats

目的:探讨自发性高血压大鼠左室肥厚与内皮功能改变间的关系以及药物改善内皮功能、抑制左室肥厚的可能性.方法:20只8周龄的SHR随机分成实验组(12只)和治疗组(8只),以8只同龄WKY作正常对照组.给予治疗组含左旋精氨酸(浓度为 7.5 g·L-1)和维生素C(浓度为4～5 g·L-1)的饮水持续12周,实验组和正常对照组给予蒸馏水饮用.20周龄的大鼠测血压后处死,常规测量心脏重量、左室重量,生化检测大鼠血浆一氧化氮水平应用HE、VG染色,结合计算机图像分析技术,检测心肌细胞直径、心肌组织胶原分数、血管周围胶原分数.结果:(1)与正常对照组相比,实验组SHR的血压增高、心率增快,左室重量指数(LVMI)显著增高,血浆一氧化氮(NO)浓度显著减小,心肌细胞直径(TDM)增大、心肌胶原分数(CVF)、血管周围胶原分数(PCA)均显著增高.两组间体重无显著性差异(P>0.05).相关分析表明:实验组SHR的LVMI与血浆NO呈负相关(r=-0.53,P<0.05),而与TDM、CVF、PCA呈正关(r=0.80、0.68、0.66,P<0.01),血浆NO与TDM、CVF、PCA呈负相关(r=-0.65、-0.54、-0.52,P<0.01 或 0.05).(2)与实验组相比,治疗组SHR的LVMI、TDM、CVF、PCA均减低,血浆NO水平增高,两组间的血压、心率、体重均无显著性差异(P>0.05).与正常对照相比,治疗组血压、心率、LVMI、TDM、CVF、PCA显著增高,而体重、血浆NO水平无显著性差异(P>0.05).结论:SHR内皮功能障碍影响心肌细胞肥大及心肌纤维化的过程是其参与影响LVH的形成的主要环节,药物改善内皮功能可以在一定程度上阻遏这一过程发展.

AIM： To explore the relationship between left ventricular hypertrophy （LVH） and endothelial function （EF） and to investigate the effects of L-Arginine and Vitamin C on LVH and EF in spontaneously hypertensive rats （SHR）. METHODS： 20 SHR with 8 weeks old were randomly divided into experiment group （12 rats） and treated group （8 rats） while 8 WKY rats were selected as a control group. The SHR of treated group received L-Arginine and Vitamin C （7.5 and 4 -5 g·L^-1 respectively in drinking water） for 12 weeks, but the WKY rats and the SHR of experiment group were given distilled water as drinking water. The rats with 20 weeks old were killed after measurements of their blood pressure and body weight. HE and VG staining combined with computed morphometry were employed to evaluate the cardiomyocyte diameter （CDM）, the collagen volume fraction （CVF）, perivascular circumferential area （PCA） on the left ventricular tissue. RESULTS： Compared with the WKY, the blood pressure was higher, heart rate was faster, left ventricular mass （LVMI） were higher, NO was lower in the experimental group. The CVF, PCA and CDM were higher in the experimental group. There were no differences in body weight between the experiment group and the control. Bivariate analysis showed that in the experiment group LVMI correlated well with NO, CVF, PCA or CDM （r =0.80, 0.68, 0.66, P 〈 0.01）. Besides, NOin the experiment group correlated well with CDM, CVF or PCA （ r = - 0.65, - 0.54, - 0.52, P 〈 0.01 or P 〈 0.05）. Compared with the experiment group, LVMI, CDM, CVF, and PCA were lower in the treated group. There was higher NO level in the treated group. There were no significant differences in blood pressure, body weight and heart rate. Compared with the control, blood pressure, heart rate, LVMI, CDM, CVF and PCA still increased. There were no significant difference in body weight and in NO between WKY and the treated group. CONCLUSIONS： LVH is related with endothelial dysfunction in SHR. The endothelial dysfunction may play a role in the development and progression of LVH by accelerating CDM and CVF and PCA increased. LL-Arginine and Vitamin C can hinder off LVH to some degree by improving endothelial function.