CAJ | 학술논문

目的探讨心肌梗死(MI)后心脏局部不同部位血管紧张素受体的分布情况及其对局部心室功能的影响,评价缬沙坦对其的调节作用,进一步阐明缬沙坦对心脏的保护机制.方法将21只犬随机分为假手术组、MI组与缬沙坦组(MI后每天给予缬沙坦10 mg/kg),后两组建立左心室前侧壁MI模型.术后4周应用组织多普勒超声检测梗死区近端心底部及远端心尖部梗死比邻的非梗死区各部位心室功能;应用免疫组织化学技术及定量逆转录-聚合酶链反应检测上述部位血管紧张素Ⅱ(AngⅡ)1型受体(AT1)和2型受体(AT2)蛋白及mRNA表达情况,假手术组在MI组对应部位取材.结果 MI组心底及心尖部AT1受体蛋白和mRNA表达量均高于假手术组(P<0.05),缬沙坦组AT1受体蛋白和mRNA表达量均低于MI组(P<0.05),心尖部低得明显.MI组心底及心尖AT2受体蛋白及mRNA表达量高于假手术组(P<0.05),缬沙坦组AT2受体蛋白和mRNA表达量均高于MI组(P<0.05).MI组心尖侧心肌收缩峰值速度(Sm)、舒张早期峰值速度(Em)和舒张晚期峰值速度(Am)较心底侧降低的比率[(心底侧-心尖侧)/心底侧](分别为79.5%±3.3%,77.3%±5.3%,86.3%±2.5%)明显大于假手术组(分别为46.7%±8.5%,36.5%±5.2%,40.7%±7.8%,均P<0.01)和缬沙坦组(分别为63.5%±5.8%,53.9%±6.6%,55.5±6.1%,均P<0.01),缬沙坦组较MI组局部心肌收缩速度明显恢复.结论 MI后压力负荷促使AT1、AT2受体蛋白及mRNA表达量增加,缬沙坦能够抑制AT1受体上调,促进AT2受体上调,对心脏起保护作用.
목적 탐토심기경사(MI)후심장국부불동부위혈관긴장소수체적분포정황급기대국부심실공능적영향,평개힐사탄대기적조절작용,진일보천명힐사탄대심장적보호궤제.방법 장21지견수궤분위가수술조、MI조여힐사탄조(MI후매천급여힐사탄10 mg/kg),후량조건립좌심실전측벽MI모형.술후4주응용조직다보륵초성검측경사구근단심저부급원단심첨부경사비린적비경사구각부위심실공능;응용면역조직화학기술급정량역전록-취합매련반응검측상술부위혈관긴장소Ⅱ(AngⅡ)1형수체(AT1)화2형수체(AT2)단백급mRNA표체정황,가수술조재MI조대응부위취재.결과 MI조심저급심첨부AT1수체단백화mRNA표체량균고우가수술조(P<0.05),힐사탄조AT1수체단백화mRNA표체량균저우MI조(P<0.05),심첨부저득명현.MI조심저급심첨AT2수체단백급mRNA표체량고우가수술조(P<0.05),힐사탄조AT2수체단백화mRNA표체량균고우MI조(P<0.05).MI조심첨측심기수축봉치속도(Sm)、서장조기봉치속도(Em)화서장만기봉치속도(Am)교심저측강저적비솔[(심저측-심첨측)/심저측](분별위79.5%±3.3%,77.3%±5.3%,86.3%±2.5%)명현대우가수술조(분별위46.7%±8.5%,36.5%±5.2%,40.7%±7.8%,균P<0.01)화힐사탄조(분별위63.5%±5.8%,53.9%±6.6%,55.5±6.1%,균P<0.01),힐사탄조교MI조국부심기수축속도명현회복.결론 MI후압력부하촉사AT1、AT2수체단백급mRNA표체량증가,힐사탄능구억제AT1수체상조,촉진AT2수체상조,대심장기보호작용.
Objective To investigate the effects of valsartan on expression of angiotensin Ⅱ receptors in different regions of heart after myocardial infarction(MI).Metbods Canines were divided into sham-operated control group(n=7),infarction group(n=7)and Valsartan group(10 mg·kg-1·day-1 for 4 weeks after MI operation,n=7).Four weeks after operation,Dopplor tissue imaging(DTI)was used to evaluate reglonal ventricular function in the noninfarcted myocardium(apical and basal near to the infarction region).The mRNA and protein expressions of angiotensin Ⅱ type 1 receptor(AT1-R)and angiotensin Ⅱ type 2 receptor(AT2-R)on the corresponding regions were detected by competitive reverse-transcriptase polymerase chain reaction technique and immunohistochemical technique respectively.Results The protein and mRNA expressions of AT1-R were significantly increased in both apical and basal regions near to the infarction in dogs with MI compared with those in control group(P<0.05)which could be down-regulated by valsartan(P<0.05).AT2-R expressions were significantly upregulated in infarction group in both apical and basal regions compared with those in control group and valsartan further increased AT2-R expressions in both areas(P<0.05). Myocardial peak systolic velocity(Sm),myocardial peak early diastolic velocity(Em)and myocardial peak late diastolic velocity(Am)at both apical and basal regions near to the infarction regions were significantly lower in MI group than those in the control group which could be significantly improved by valsartan.Conclusion Both mRNA and protein expressions of AT1-R and AT2-R are upregulated in noninfarcted regions near MI,valsartan improved myocardial function via inhibiting AT1-R upregulation and enhancing AT2-R upregulation.