中华心血管病杂志
中華心血管病雜誌
중화심혈관병잡지
Chinese Journal of Cardiology
2011年
8期
706-710
,共5页
宋衍秋%赵莉莉%毛用敏%赵鸿铭%曹丽%崔丽%崔让庄
宋衍鞦%趙莉莉%毛用敏%趙鴻銘%曹麗%崔麗%崔讓莊
송연추%조리리%모용민%조홍명%조려%최려%최양장
心力衰竭,充血性%利钠肽,脑%心室功能,左%基因疗法
心力衰竭,充血性%利鈉肽,腦%心室功能,左%基因療法
심력쇠갈,충혈성%리납태,뇌%심실공능,좌%기인요법
Heart failure,congestive%Natriuretic peptide,brain%Ventricular function,left%Gene therapy
目的 观察外源基因人B型利钠肽对慢性心力衰竭(心衰)大鼠心功能的影响.方法 30只入选心衰大鼠,随机分为携带人B型利钠肽基因重组腺病毒组(Ad-hBNP组)、重组空白腺病毒组(Ad-Track组)、生理盐水组(NS组),另设不予任何治疗的假手术组作为对照;分别经腹腔注射予以相应治疗,每周1次,共4周.4周后实验动物行超声心动图、血流动力学检测,酶联免疫吸附试验检测血清外源基因人B型利钠肽水平,全心质量指数检测.结果 间断Ad-hBNP治疗后,Ad-hBNP组心衰大鼠室间隔厚度、左室后壁厚度、左室舒张末径、左室收缩末径[(2.34±0.29)mm、(2.28±0.18)mm、(6.50±0.42)mm、(3.54±0.59)mm]显著低于Ad-Track组[(2.71±0.35)mm、(3.02±0.85)mm、(7.71±0.83)mm、(4.72±0.80)mm,均为P＜0.05]和NS组[(2.78±0.23)mm、(2.83±0.53)mm、(7.34±0.97)mm、(4.55±0.77)mm,均为P＜0.05],而左室射血分数、左室短轴缩短率[(79.27±7.01)%、(43.38±6.73)%]显著高于Ad-Track组[(70.85±4.81)%、(35.72±3.68)%,均为P＜0.01]和NS组[(69.67±6.90)%、(34.91±5.10)%,均为P＜0.01].Ad-hBNP组与Ad-Track组和NS组比较:心率显著降低,左室收缩压显著升高[为(131.79±15.76)mm Hg(1 mm Hg=0.133 kPa)、(112.99±32.35)mm Hg、(117.13±15.26)mm Hg],左室内压最大上升速率显著升高[分别为(5037.20±430.41)mm Hg/s、(4217.40±1354.15)mm Hg/s、(4310.50±1293.97)mm Hg/s;P＜0.05];左室内压最大下降速率显著升高[分别为(-4382.00±1304.79)mm Hg/s、(-3725.00±791.34)mm Hg/s、(-3890.00±1043.73)mm Hg/s,均为P＜0.05];左室舒张末压降低[分别为(-4.24±4.00)mm Hg、(21.99±6.80)mm Hg、(18.00±12.25)mm Hg,均为P＜0.01];心脏质量及全心质量指数均降低.结论 间断给予Ad-hBNP能够有效地改善心衰大鼠心脏结构和功能.
目的 觀察外源基因人B型利鈉肽對慢性心力衰竭(心衰)大鼠心功能的影響.方法 30隻入選心衰大鼠,隨機分為攜帶人B型利鈉肽基因重組腺病毒組(Ad-hBNP組)、重組空白腺病毒組(Ad-Track組)、生理鹽水組(NS組),另設不予任何治療的假手術組作為對照;分彆經腹腔註射予以相應治療,每週1次,共4週.4週後實驗動物行超聲心動圖、血流動力學檢測,酶聯免疫吸附試驗檢測血清外源基因人B型利鈉肽水平,全心質量指數檢測.結果 間斷Ad-hBNP治療後,Ad-hBNP組心衰大鼠室間隔厚度、左室後壁厚度、左室舒張末徑、左室收縮末徑[(2.34±0.29)mm、(2.28±0.18)mm、(6.50±0.42)mm、(3.54±0.59)mm]顯著低于Ad-Track組[(2.71±0.35)mm、(3.02±0.85)mm、(7.71±0.83)mm、(4.72±0.80)mm,均為P＜0.05]和NS組[(2.78±0.23)mm、(2.83±0.53)mm、(7.34±0.97)mm、(4.55±0.77)mm,均為P＜0.05],而左室射血分數、左室短軸縮短率[(79.27±7.01)%、(43.38±6.73)%]顯著高于Ad-Track組[(70.85±4.81)%、(35.72±3.68)%,均為P＜0.01]和NS組[(69.67±6.90)%、(34.91±5.10)%,均為P＜0.01].Ad-hBNP組與Ad-Track組和NS組比較:心率顯著降低,左室收縮壓顯著升高[為(131.79±15.76)mm Hg(1 mm Hg=0.133 kPa)、(112.99±32.35)mm Hg、(117.13±15.26)mm Hg],左室內壓最大上升速率顯著升高[分彆為(5037.20±430.41)mm Hg/s、(4217.40±1354.15)mm Hg/s、(4310.50±1293.97)mm Hg/s;P＜0.05];左室內壓最大下降速率顯著升高[分彆為(-4382.00±1304.79)mm Hg/s、(-3725.00±791.34)mm Hg/s、(-3890.00±1043.73)mm Hg/s,均為P＜0.05];左室舒張末壓降低[分彆為(-4.24±4.00)mm Hg、(21.99±6.80)mm Hg、(18.00±12.25)mm Hg,均為P＜0.01];心髒質量及全心質量指數均降低.結論 間斷給予Ad-hBNP能夠有效地改善心衰大鼠心髒結構和功能.
목적 관찰외원기인인B형리납태대만성심력쇠갈(심쇠)대서심공능적영향.방법 30지입선심쇠대서,수궤분위휴대인B형리납태기인중조선병독조(Ad-hBNP조)、중조공백선병독조(Ad-Track조)、생리염수조(NS조),령설불여임하치료적가수술조작위대조;분별경복강주사여이상응치료,매주1차,공4주.4주후실험동물행초성심동도、혈류동역학검측,매련면역흡부시험검측혈청외원기인인B형리납태수평,전심질량지수검측.결과 간단Ad-hBNP치료후,Ad-hBNP조심쇠대서실간격후도、좌실후벽후도、좌실서장말경、좌실수축말경[(2.34±0.29)mm、(2.28±0.18)mm、(6.50±0.42)mm、(3.54±0.59)mm]현저저우Ad-Track조[(2.71±0.35)mm、(3.02±0.85)mm、(7.71±0.83)mm、(4.72±0.80)mm,균위P＜0.05]화NS조[(2.78±0.23)mm、(2.83±0.53)mm、(7.34±0.97)mm、(4.55±0.77)mm,균위P＜0.05],이좌실사혈분수、좌실단축축단솔[(79.27±7.01)%、(43.38±6.73)%]현저고우Ad-Track조[(70.85±4.81)%、(35.72±3.68)%,균위P＜0.01]화NS조[(69.67±6.90)%、(34.91±5.10)%,균위P＜0.01].Ad-hBNP조여Ad-Track조화NS조비교:심솔현저강저,좌실수축압현저승고[위(131.79±15.76)mm Hg(1 mm Hg=0.133 kPa)、(112.99±32.35)mm Hg、(117.13±15.26)mm Hg],좌실내압최대상승속솔현저승고[분별위(5037.20±430.41)mm Hg/s、(4217.40±1354.15)mm Hg/s、(4310.50±1293.97)mm Hg/s;P＜0.05];좌실내압최대하강속솔현저승고[분별위(-4382.00±1304.79)mm Hg/s、(-3725.00±791.34)mm Hg/s、(-3890.00±1043.73)mm Hg/s,균위P＜0.05];좌실서장말압강저[분별위(-4.24±4.00)mm Hg、(21.99±6.80)mm Hg、(18.00±12.25)mm Hg,균위P＜0.01];심장질량급전심질량지수균강저.결론 간단급여Ad-hBNP능구유효지개선심쇠대서심장결구화공능.
Objective To evaluate the therapeutic effect of hBNP on rats with chronic heart failure (CHF). Methods Thirty CHF rats defined by echocardiography at 12 weeks post abdominal aortic constriction were randomly divided into Ad-hBNP group (2. 5 × 1010 VP/ml NS Ad-hBNP 1 ml/week ×4,n = 14), Ad-Track group ( n = 8 ), placebo group ( NS, n = 8 ), 10 sham-operated rats served as control group. After 4 weeks treatment, cardiac function was evaluated by echocardiography and hemodynamic measurements. Heart weight (HW) and HW/body weight (BW) ratio were determined. Results IVS,LVPW, LVEDD and LVESD were significantly reduced in the Ad-hBNP group [(2. 34 ±0. 29)mm, (2. 28 ± 0. 18)mm, (6. 50 ±0. 42)mm, (3.54 ±0. 59) mm] than those in the Ad-Track group[(2. 71 ±0. 35) mm,(3.02 ±0.85)mm, (7.71 ±0.83)mm, (4.72 ±0.80)mm] and in the NS group [(2.78 ±0.23)mm,(2. 83 ± 0. 53 ) mm, (7. 34 ± 0. 97 ) mm, (4. 55 ± 0. 77 ) mm, all P ＜ 0. 05]. The LVEF and LVFS of the Ad-hBNP group [(79. 27 ±7.01 )%, (43.38 ±6. 73)%] were significantly higher than in the Ad-Track group[(70.85±4.81)%, (35.72 ±3.68)%] and in the NS group[(69.67 ±6.90)%, (34.91 ±5.10)%, all P ＜0. 01]. HR[(417.48 ±32. 57) beats/min, (446. 85 ±61.49) beats/min, P ＜0. 05;(440. 83 ±32. 18) beats/min , P ＜0. 05], LVEDP[( - 4. 24 ±4. 00) mm Hg( 1 mm Hg =0. 133 kPa);(21.99 ±6. 80) mm Hg, P ＜0. 01; ( 18.00 ± 12. 25)mm Hg, P＜0. 01] were significantly decreased and while LVSP[(131.79 ±15.76) mm Hg; (112.99 ±32.35) mm Hg, P＜0.05; (117.13 ±15.26)mmHg], +dP/dtmax[(5037.20 ±430.41) mm Hg/s; (4217.40 ± 1354. 15)mm Hg/s, P ＜0.05;(4310. 50 ± 1293.97 ) mm Hg/s, P ＜ 0. 05] and - dP/dtmax [( - 4382. 00 ± 1304. 79 ) mm Hg/s;(-3725.00±791.34) mm Hg/s, P ＜ 0.05; ( - 3890.00 ± 1043.73) mm Hg/s, P ＜ 0.05] were significantly increased in Ad-hBNP group than in Ad-Track group and NS group ( all P ＜ 0. 05 ). HW and HW/BW were also decreased in Ad-hBNP group than in the Ad-Track group and the NS group. Conclusion Exogenous hBNP improved the cardiac function and attenuated remodeling in CHF rats.
