[关键词]
[摘要]
目的 探究注射用益气复脉(冻干)(YQFM)对心衰合并低血压大鼠的血压、心功能以及相应生化指标的影响。方法 将SD大鼠进行冠状动脉左前降支手术结扎制备心衰模型,饲养2周后,用小动物超声仪检测大鼠心功能筛选造模成功的大鼠,假手术组进行开胸手术不结扎。心衰大鼠血压最低(均低于90 mmHg)的10只挑选出来作为非药物性低血压-YQFM(470 mg/kg)组,其余大鼠进行呋塞米(53.35 mg/kg)低血压造模1周(与给药前比较,血压下降幅度在20 mmHg左右)后,随机分为模型组(呋塞米53.35 mg/kg),联合给药:呋塞米(53.35 mg/kg)+YQFM低、高剂量(470、940 mg/kg)组,YQFM低、高剂量(470、940 mg/kg)组,各给药组分别ig呋塞米或(和)iv YQFM,给药2周。超声诊断仪检测大鼠的心功能;检测大鼠心脏指数(HWI);从术后1周开始至给药结束监测大鼠血压变化;ELISA法检测各组大鼠血清脑钠肽(BNP)、心钠素(ANP)、血管紧张素Ⅱ(AngⅡ)、白介素-6(IL-6)、肌酸激酶同工酶(MB)、β1肾上腺素受体(β1AR)含量变化。结果 模型组大鼠心脏有明显的前壁运动异常,而给药各组心室收缩功能障碍具有不同程度的减轻。与模型组比较,给药组的E/A值>1.2的大鼠占比明显上升;与模型组比较,非药物性低血压-YQFM组,YQFM低、高剂量组,呋塞米+YQFM低、高剂量组LVEF、LVFS均显著升高,差异有统计学意义(P<0.05、0.01)。与模型组比较,各给药组HWI均显著降低(P<0.05、0.01)。低血压造模实验后,各组血压显著降低(P<0.01),治疗给药后,各给药组的血压显著升高(P<0.01)。与模型组比较,给药组的BNP、ANP、IL-6、MB和AngⅡ水平显著下降(P<0.01),而β1AR水平显著升高(P<0.01)。结论 YQFM可以有效升高心衰大鼠血压,也能有效地减轻呋塞米用药引起的低血压;YQFM能显著改善心衰大鼠生化指标水平,抑制肾素-血管紧张素系统(RAS)的过度激活,改善炎症症状,从而改善大鼠的心衰症状。
[Key word]
[Abstract]
Objective To investigate the effects of Yiqi Fumai Lyophilized Injection (YQFM) on blood pressure, cardiac function and corresponding biochemical parameters for rats with heart failure and hypotension. Methods The SD rats were subjected to ligating the anterior descending branch of the left coronary artery. After feeding two weeks later, the heart function of the rats was detected by diasonograph and the rats with successful heart failure were picked up to be treated. The sham operation group underwent thoracotomy without ligation. Totally ten heart failure rats with the lowest blood pressure (all lower than 90 mmHg) were selected as the non drug hypotension YQFM (470 mg/kg) group. The rest of the rats were subjected to furosemide (53.35 mg/kg) hypotension model for one week (compared with before administration, the blood pressure decreased by about 20 mmHg), They were randomly divided into model group (furosemide 53.35 mg/kg), furosemide (53.35 mg/kg) + YQFM low and high dose (470, 940 mg/kg) groups, YQFM low and high dose (470, 940 mg/kg) groups, each group was given furosemide by ig or (and) YQFM by iv for two weeks. After 14 days of administration, the cardiac function of the rats in each group was detected by diasonograph and their heart index (HWI) were examined. Blood pressure were measured from one week after operation to the end of administration. The serum levels of brain natriuretic peptide (BNP), atrial natriuretic peptide (ANP), angiotensin Ⅱ (Ang Ⅱ), interleukin-6 (IL-6), creatine kinase isoenzyme (MB) and β 1-adrenergic receptor (β 1ar) were detected by ELISA. Results In the model group, the anterior wall motion was obviously abnormal, and the ventricular systolic dysfunction was alleviated in different degrees. Compared with the model group, the proportion of rats with E/A value > 1.2 in the treatment group was significantly increased; compared with the model group, LVEF and LVFS in the non drug hypotension YQFM group, YQFM low and high dose groups, furosemide + YQFM low and high dose groups were significantly increased, the differences were statistically significant (P<0.05, 0.01). Compared with the model group, the HWI of each treatment group was significantly decreased (P<0.05, 0.01). After hypotensive modeling, the blood pressures of the rats in each group were decreased significantly (P<0.01). After treatment, the blood pressure of the rats in each group was significantly increased (P<0.01). In addition, comparing to the model group, the levels of brain natriuretic peptide (BNP), atrial natriuretic peptide (ANP), interleukin-6 (IL-6), myoglobin (MB), and angiotensin II (Ang II) of the rats in the drugadministered group were significantly decreased (P<0.01). While the β1 adrenergic receptor (β1AR) level of these rats was significantly increased (P<0.01). Conclusion The blood pressure of CHF rats in the YQFM group could be effectively increased and their hypotensions caused by Furosemide were improved effectively (P<0.01). The biochemical indicators level of the rats in the drug-administered group could be improved significantly, the excessive activation of the renin-angiotensin system (RAS) of these rats were inhibited effectively, and their symptoms of inflammation were improved effectively, thereby the symptoms of heart failure in rats were improved.
[中图分类号]
R965
[基金项目]
天津市科技计划项目(18YFCZZC00430)