目的 探究注射用益氣復(fù)脈（凍干）（YQFM）對心衰合并低血壓大鼠的血壓、心功能以及相應(yīng)生化指標(biāo)的影響。方法 將SD大鼠進(jìn)行冠狀動脈左前降支手術(shù)結(jié)扎制備心衰模型，飼養(yǎng)2周后，用小動物超聲儀檢測大鼠心功能篩選造模成功的大鼠，假手術(shù)組進(jìn)行開胸手術(shù)不結(jié)扎。心衰大鼠血壓最低（均低于90 mmHg）的10只挑選出來作為非藥物性低血壓-YQFM（470 mg/kg）組，其余大鼠進(jìn)行呋塞米（53.35 mg/kg）低血壓造模1周（與給藥前比較，血壓下降幅度在20 mmHg左右）后，隨機分為模型組（呋塞米53.35 mg/kg），聯(lián)合給藥：呋塞米（53.35 mg/kg）+YQFM低、高劑量（470、940 mg/kg）組，YQFM低、高劑量（470、940 mg/kg）組，各給藥組分別ig呋塞米或（和）iv YQFM，給藥2周。超聲診斷儀檢測大鼠的心功能；檢測大鼠心臟指數(shù)（HWI）；從術(shù)后1周開始至給藥結(jié)束監(jiān)測大鼠血壓變化；ELISA法檢測各組大鼠血清腦鈉肽（BNP）、心鈉素（ANP）、血管緊張素Ⅱ（AngⅡ）、白介素-6（IL-6）、肌酸激酶同工酶（MB）、β1腎上腺素受體（β1AR）含量變化。結(jié)果 模型組大鼠心臟有明顯的前壁運動異常，而給藥各組心室收縮功能障礙具有不同程度的減輕。與模型組比較，給藥組的E/A值>1.2的大鼠占比明顯上升；與模型組比較，非藥物性低血壓-YQFM組，YQFM低、高劑量組，呋塞米+YQFM低、高劑量組LVEF、LVFS均顯著升高，差異有統(tǒng)計學(xué)意義（P<0.05、0.01）。與模型組比較，各給藥組HWI均顯著降低（P<0.05、0.01）。低血壓造模實驗后，各組血壓顯著降低（P<0.01），治療給藥后，各給藥組的血壓顯著升高（P<0.01）。與模型組比較，給藥組的BNP、ANP、IL-6、MB和AngⅡ水平顯著下降（P<0.01），而β1AR水平顯著升高（P<0.01）。結(jié)論 YQFM可以有效升高心衰大鼠血壓，也能有效地減輕呋塞米用藥引起的低血壓；YQFM能顯著改善心衰大鼠生化指標(biāo)水平，抑制腎素-血管緊張素系統(tǒng)（RAS）的過度激活，改善炎癥癥狀，從而改善大鼠的心衰癥狀。

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.

R965

天津市科技計劃項目（18YFCZZC00430）