抑郁对急性心肌梗死大鼠心室重构的影响及其机制探讨
억욱대급성심기경사대서심실중구적영향급기궤제탐토
Effect of depressive disorder on ventricular remodeling and its mechanism in acute myocardial infarction rats
  • 万方数据
    中华老年医学杂志 중화노년의학잡지
    Chinese Journal of Geriatrics
    2010年 11期 944-948 ,共5页

    胡国义%周大亮%魏林%赵学忠

    호국의%주대량%위림%조학충

    抑郁症%心肌梗死%心室重构 抑鬱癥%心肌梗死%心室重構
    억욱증%심기경사%심실중구
    Depressive Disorder%Myocardial infarction%Ventricular remodeling
    目的 观察抑郁对急性心肌梗死大鼠心室重构及抗氧化能力的影响. 方法 实验大鼠46只,随机分为4组:假手术组(10只),梗死模型组(12只)、抑郁模型组(12只)、路优泰组(12只).路优泰组给予每天路优泰90mg/kg给药4周后用Open-field法观察各组大鼠行为学变化以及测定血管紧张素Ⅱ(AgⅡ)、醛固酮、丙二醛(MDA)、超氧化物歧化酶(SOD)值和光镜、电镜下观察心肌组织切片. 结果 与假手术组比较,抑郁模型组水平穿越格数、竖立次数、理毛时间均减少,中央格停留时间、粪便粒数均增加;与抑郁模型组比较,梗死模型型组、路优泰组水平穿越格数、竖立次数、理毛时间明显增加,中央格停留时间、粪便粒数明显减少(F值分别为16.9、44.56、71.79、34.86、29.18,均P＜0.01).实验第4周各组大鼠左室相对重量、右室相对重量、室间隔厚度假手术组分别为(1.63±0.15)mg/g、(0.48±0.10)mg/g、(1.75±0.38)mm,梗死模型组分别为(2.06±0.21)mg/g、(0.62±0.10)mg/g、(2.25±0.30)mm,抑郁模型组分别为(2.90±0.47)mg/g、(1.00±0.28)mg/g、(2.58±0.34)mm,路优泰组分别为(2.20±0.34)mg/g、(0.67±0.15)mg/g、(2.25±0.23)mm,与假手术组比较,梗死模型组、抑郁模型组、路优泰组,左室相对重量、右室相对重量、室间隔厚度明显增加,与抑郁模型组比较,梗死模型组、路优泰组左室相对重量、右室相对重量、室间隔厚度减少(F值分别为6.31、21.9、115.7、9.19,均P＜0.05).并且抑郁可加重心肌水肿及超微结构损伤.实验第4周AgⅡ、醛固酮、丙二醛、SOD值,抑郁组大鼠分别为(1957.5±662.6)ng/L、(0.453±0.111)ng/L(16.00±3.03)nmol/L、(80.57±7.00)U/ml,假手术组大鼠分别为(1143.8±98.0)ng/L、(0.198±0.087)ng/L、(8.03±0.44)nmol/L、(95.20±4.87)U/ml,梗死模型组大鼠分别为(1407.5±255.8)ng/L、(0.295±0.027)ng/L、(11.18±4.30)nmol/L、(87.33±3.51)U/ml,路优泰组(1400.0±239.0)ng/L、(0.326±0.073)ng/L、(11.88±3.36)nmol/L、(89.13±0.17)U/ml,抑郁组大鼠4周后,AgⅡ、醛固酮、丙二醛数值明显高于各组,而SOD值低于各组(F值分别为6.58、11.9、11.39、8.82,P＜0.05). 结论 心肌梗死后抑郁可加重大鼠急性心肌梗死后心室重构及降低机体抗氧化能力.
    목적 관찰억욱대급성심기경사대서심실중구급항양화능력적영향. 방법 실험대서46지,수궤분위4조:가수술조(10지),경사모형조(12지)、억욱모형조(12지)、로우태조(12지).로우태조급여매천로우태90mg/kg급약4주후용Open-field법관찰각조대서행위학변화이급측정혈관긴장소Ⅱ(AgⅡ)、철고동、병이철(MDA)、초양화물기화매(SOD)치화광경、전경하관찰심기조직절편. 결과 여가수술조비교,억욱모형조수평천월격수、수립차수、리모시간균감소,중앙격정류시간、분편립수균증가;여억욱모형조비교,경사모형형조、로우태조수평천월격수、수립차수、리모시간명현증가,중앙격정류시간、분편립수명현감소(F치분별위16.9、44.56、71.79、34.86、29.18,균P＜0.01).실험제4주각조대서좌실상대중량、우실상대중량、실간격후도가수술조분별위(1.63±0.15)mg/g、(0.48±0.10)mg/g、(1.75±0.38)mm,경사모형조분별위(2.06±0.21)mg/g、(0.62±0.10)mg/g、(2.25±0.30)mm,억욱모형조분별위(2.90±0.47)mg/g、(1.00±0.28)mg/g、(2.58±0.34)mm,로우태조분별위(2.20±0.34)mg/g、(0.67±0.15)mg/g、(2.25±0.23)mm,여가수술조비교,경사모형조、억욱모형조、로우태조,좌실상대중량、우실상대중량、실간격후도명현증가,여억욱모형조비교,경사모형조、로우태조좌실상대중량、우실상대중량、실간격후도감소(F치분별위6.31、21.9、115.7、9.19,균P＜0.05).병차억욱가가중심기수종급초미결구손상.실험제4주AgⅡ、철고동、병이철、SOD치,억욱조대서분별위(1957.5±662.6)ng/L、(0.453±0.111)ng/L(16.00±3.03)nmol/L、(80.57±7.00)U/ml,가수술조대서분별위(1143.8±98.0)ng/L、(0.198±0.087)ng/L、(8.03±0.44)nmol/L、(95.20±4.87)U/ml,경사모형조대서분별위(1407.5±255.8)ng/L、(0.295±0.027)ng/L、(11.18±4.30)nmol/L、(87.33±3.51)U/ml,로우태조(1400.0±239.0)ng/L、(0.326±0.073)ng/L、(11.88±3.36)nmol/L、(89.13±0.17)U/ml,억욱조대서4주후,AgⅡ、철고동、병이철수치명현고우각조,이SOD치저우각조(F치분별위6.58、11.9、11.39、8.82,P＜0.05). 결론 심기경사후억욱가가중대서급성심기경사후심실중구급강저궤체항양화능력.
    Objective To observe the effect of depressive disorder on ventricular remodeling and its mechanism in acute myocardial infarction (AMI) rats. Methods Forty-six AMI Wistar rats were randomly divided into sham-operation (n=10), AMI (n=12), depression (n=12), neurostan by open field test, and the detection of angiotensin Ⅱ (Ag Ⅱ ), aldosterone (ALD), malondialdehyde (MDA), superoxide dismutase (SOD) were performed, the pathological sections were observed under light and electron microscopes. Results Compared with sham-operation group, depression group had decreased values of squares crossing times, rearing times and grooming time, increased time of staying in the central square and defecation. Compared with depression group, AMI and neurostan treatment groups had increased values of squares crossing times, rearing times and grooming time,decreased time of staying in the central square and defecation (F=16. 9, 44.56, 71.79, 34.86,29. 18, P＜0.01). At the 4 week of test, the left and right ventricular relative weights (LVRW,RVRW) and thickness of interventricular septum were (1.63±0.15) mg/g, (0. 48±0. 10) mg/g and (1.75 ± 0. 38) mm in sham-operation group, the corresponding data were (2.06±0.21) mg/g,(0.62±0.10) mg/g and (2.25±0.30) mm in AMI group, (2.90±0.47) mg/g, (1.00±0.28) mg/gand (2.58±0.34) mm in depression group, (2.20±0.34) mg/g, (0.67±0.15) mg/g and (2. 25±0.23) mm in neurostan treatment group. Compared with sham-operation group, AMI, depression and neurostan groups had obviously increased values of LVRW, RVRW and thickness of interventricular septum. Compared with depression group, AMI and neurostan groups had decreased LVRW, RVRW and thickness of interventricular septum (F=6.31, 21.9, 115.7, 9.91, P＜0.05). And the depression also could aggravate edema and injury of ultrastructure in myocardial tissue. The values of AgⅡ , ALD, MDA and SOD were (1957.5±662.6) ng/L, (0.453±0.111) ng/L, (16. 00±3.03)nmol/L and (80.57 ± 7.00) U/ml in depression group, the corresponding data were (1143.8± 98.0)ng/L, (0.198±0.087) ng/L, (8.03 ± 0.44 ) nmol/L and (95.20 ± 4.87) U/ml in sham-operated group, (1407.5±255.8) ng/L, (0.295±0.027) ng/L, (11.18±4.30) nmol/L and (87.33±3.51)U/ml in AMI group, (1400.0±239.0) ng/L, (0.326±0.073) ng/L, (11.88±3.36) nmol/L and (89.13 ±0.17) U/ml in neurostan group. After 4 weeks, the values of Ag Ⅱ , ALD and MDA increased in depression group while the level of SOD reduced (F=6.58, 11.9, 11.39, 8. 82, P＜0.05). Conclusions Depressive disorder after AMI in rats can aggravate ventricular remodeling and lower the ability of antioxygen.
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