国际呼吸杂志
國際呼吸雜誌
국제호흡잡지
INTERNATIONAL JOURNAL OF RESPIRATION
2012年
15期
1158-1161
,共4页
赵瑛娟%胡晓芸%杜永成%邢爱萍%秦艳艳
趙瑛娟%鬍曉蕓%杜永成%邢愛萍%秦豔豔
조영연%호효예%두영성%형애평%진염염
烟雾暴露%肺动脉压%一氧化氮%内皮型一氧化氮合酶
煙霧暴露%肺動脈壓%一氧化氮%內皮型一氧化氮閤酶
연무폭로%폐동맥압%일양화담%내피형일양화담합매
Cigarette smoke exposure%Pulmonary artery pressure%Nitric oxide%Endothelium nitric oxide synthase
目的 探讨不同烟雾暴露量对大鼠肺动脉压及肺血管内皮型一氧化氮合酶(eNOS)和一氧化氮(NO)表达的影响.方法 健康雄性SD大鼠21只,随机分为对照组(C组)、烟雾暴露1个月组(S1m组)、烟雾暴露3个月组(S3m组),建立大鼠被动吸烟模型.检测各组大鼠平均右心室收缩压(mRVSP)及右心室肥大指数(RVHI),硝酸还原酶法检测肺组织NO的表达,免疫组化法检测肺血管eNOS的表达.结果 ①S3m组mRVSP及RVHI[(65.63±0.93)mmHg,(54.79±7.13)％]高于S1m组[(23.57±14.51)mmHg,(36.62±1.32)％]与C组[(16.85±1.26)mmHg,(32.41±0.26)％],差异均有统计学意义(P值均＜0.01),C组与S1m组差异无统计学意义(P＞0.05)；②S1m组与S3m组肺血管内皮细胞eNOS蛋白(0.32±0.04,0.24±0.03)均低于C组(0.43±0.06),差异均有统计学意义(P值均＜0.01),S3m组低于S1m组,差异有统计学意义(P＜0.01)；③S1m组和S3m组肺组织NO[(1.98±0.20)μmol/gprot,(0.95±0.09)μmol/gprot]均低于C组[(2.98±0.19)μmol/gprot],差异均有统计学意义(P值均＜0.01),S3m组低于S1m组,差异有统计学意义(P＜0.01);④mRVSP与RVHI呈正相关(r=0.713,P＜0.01),肺组织NO与mRVSP呈负相关(r=-0.615,P＜0.05),肺血管eNOS与肺组织NO呈正相关(r=0.944,P＜0.01).结论 烟雾暴露可能下调大鼠肺血管内皮细胞eNOS的表达,进而影响NO的合成,参与肺动脉压高压的形成,且该作用在一定范围内呈时间依赖性.
目的 探討不同煙霧暴露量對大鼠肺動脈壓及肺血管內皮型一氧化氮閤酶(eNOS)和一氧化氮(NO)錶達的影響.方法 健康雄性SD大鼠21隻,隨機分為對照組(C組)、煙霧暴露1箇月組(S1m組)、煙霧暴露3箇月組(S3m組),建立大鼠被動吸煙模型.檢測各組大鼠平均右心室收縮壓(mRVSP)及右心室肥大指數(RVHI),硝痠還原酶法檢測肺組織NO的錶達,免疫組化法檢測肺血管eNOS的錶達.結果 ①S3m組mRVSP及RVHI[(65.63±0.93)mmHg,(54.79±7.13)％]高于S1m組[(23.57±14.51)mmHg,(36.62±1.32)％]與C組[(16.85±1.26)mmHg,(32.41±0.26)％],差異均有統計學意義(P值均＜0.01),C組與S1m組差異無統計學意義(P＞0.05)；②S1m組與S3m組肺血管內皮細胞eNOS蛋白(0.32±0.04,0.24±0.03)均低于C組(0.43±0.06),差異均有統計學意義(P值均＜0.01),S3m組低于S1m組,差異有統計學意義(P＜0.01)；③S1m組和S3m組肺組織NO[(1.98±0.20)μmol/gprot,(0.95±0.09)μmol/gprot]均低于C組[(2.98±0.19)μmol/gprot],差異均有統計學意義(P值均＜0.01),S3m組低于S1m組,差異有統計學意義(P＜0.01);④mRVSP與RVHI呈正相關(r=0.713,P＜0.01),肺組織NO與mRVSP呈負相關(r=-0.615,P＜0.05),肺血管eNOS與肺組織NO呈正相關(r=0.944,P＜0.01).結論 煙霧暴露可能下調大鼠肺血管內皮細胞eNOS的錶達,進而影響NO的閤成,參與肺動脈壓高壓的形成,且該作用在一定範圍內呈時間依賴性.
목적 탐토불동연무폭로량대대서폐동맥압급폐혈관내피형일양화담합매(eNOS)화일양화담(NO)표체적영향.방법 건강웅성SD대서21지,수궤분위대조조(C조)、연무폭로1개월조(S1m조)、연무폭로3개월조(S3m조),건립대서피동흡연모형.검측각조대서평균우심실수축압(mRVSP)급우심실비대지수(RVHI),초산환원매법검측폐조직NO적표체,면역조화법검측폐혈관eNOS적표체.결과 ①S3m조mRVSP급RVHI[(65.63±0.93)mmHg,(54.79±7.13)％]고우S1m조[(23.57±14.51)mmHg,(36.62±1.32)％]여C조[(16.85±1.26)mmHg,(32.41±0.26)％],차이균유통계학의의(P치균＜0.01),C조여S1m조차이무통계학의의(P＞0.05)；②S1m조여S3m조폐혈관내피세포eNOS단백(0.32±0.04,0.24±0.03)균저우C조(0.43±0.06),차이균유통계학의의(P치균＜0.01),S3m조저우S1m조,차이유통계학의의(P＜0.01)；③S1m조화S3m조폐조직NO[(1.98±0.20)μmol/gprot,(0.95±0.09)μmol/gprot]균저우C조[(2.98±0.19)μmol/gprot],차이균유통계학의의(P치균＜0.01),S3m조저우S1m조,차이유통계학의의(P＜0.01);④mRVSP여RVHI정정상관(r=0.713,P＜0.01),폐조직NO여mRVSP정부상관(r=-0.615,P＜0.05),폐혈관eNOS여폐조직NO정정상관(r=0.944,P＜0.01).결론 연무폭로가능하조대서폐혈관내피세포eNOS적표체,진이영향NO적합성,삼여폐동맥압고압적형성,차해작용재일정범위내정시간의뢰성.
Objective To explore the effects of cigarette smoke exposure on pulmonary artery pressure and levels of endothelium nitric oxide synthase (eNOS) and nitric oxide (NO) of pulmonary vascular in rats.Methods Twenty-one male SD rats were divided randomly into control group (C group),smoke exposure one month group (S1m group) and smoke exposure three months group (S3m group),seven rats in each group.Mean right ventricular systolic pressure (mRVSP) and right ventricular hypertrophy index (RVHI) were observed.Nitrate reductase enzymatic was employed to detect the expression of NO in lung tissue.The expression of eNOS protein in pulmonary vascular was measured by immunohistochemistry.Results ① The mRVSP and RVHI in S3m group [(65.63 ± 0.93) mmHg,( 54.79 ± 7.13) ％]were significantly higher than those in S1 m group [ ( 23.57 ± 14.51 ) mm Hg,(36.62 ±1.32)％]and C group [(16.85±1.26) mmHg,(32.41±0.26)％](all P＜0.01).There were no statistical difference in mRVSP and RVHI between C group and S1m group ( P ＞0.05).②The eNOS protein expression of pulmonary vascular in SIm group and S3m group (0.32 ±0.04,0.24 ±0.03) were lower than that in group C (0.43 ± 0.06) (all P ＜0.01),and that in S3m group was lower than that in S1m group ( P ＜0.01).③The NO expression of lung tissue in S1m group and S3m group[ (1.98±0.20) μmol/gprot,(0.95± 0.09) μmol/gprot]was lower than that in group C [(2.98±0.19) μmol/gprot](all P ＜ 0.01 ),and that in S3m group was less than that in S1m group ( P ＜ 0.01 ).④ mRVSP was positively correlated with RVHI (r =0.713,P ＜0.01).NO in lung tissue was negatively correlated with mRVSP ( r=-0.615,P＜0.05).eNOS in pulmonary vascular was positively associated with NO in lung tissue ( r =0.944,P ＜ 0.01).Conclusions By down-regulating the expression of eNOS protein in endothelial cell of pulmonary vascular,cigarette smoke exposure induces the biosynthesis of NO,which induces the increase of pulmonary artery pressure,and the effect is time dependence in certain scope.
