广西医学
廣西醫學
엄서의학
GUANGXI MEDICAL JOURNAL
2013年
4期
418-421
,共4页
郑晓宇%覃家锦%李波%何巍%冯旭
鄭曉宇%覃傢錦%李波%何巍%馮旭
정효우%담가금%리파%하외%풍욱
肺动脉高压%血管重构%新生内膜%磷酸二酯酶%动物模型%大鼠
肺動脈高壓%血管重構%新生內膜%燐痠二酯酶%動物模型%大鼠
폐동맥고압%혈관중구%신생내막%린산이지매%동물모형%대서
Pulmonary hypertension%Vascular remodeling%Neointima%Phosphodiesterase%Animal model%Rat
目的以左肺切除(PE)+野百合碱(MCT)建立大鼠肺动脉高压(PAH)新生内膜模型,探讨磷酸二酯酶1C(PDE1C)在该模型肺组织中的表达水平及作用.方法采用单纯PE、MCT、PE+MCT(P+M)3种方法建立大鼠PAH模型;检测模型大鼠平均肺动脉压力(mPAP)、中膜厚度百分比、右心肥厚指数(RV/LV+S)比值,观察新生内膜形成和非肌性小动脉肌化程度,比较3种PAH动物模型肺血管重构模式的差异;采用免疫组化检测PDE1C在3种动物模型肺组织中的表达水平.结果P+M组右肺腺泡内血管出现新生内膜病变,且动物出现严重右心室肥大,肺动脉中膜增厚,平均mPAP和无肌性血管肌化程度较其他模型显著增加.大鼠PAH新生内膜模型PDE1C蛋白表达显著增加(P<0.05).结论P+M模型能更好地模拟人类严重PAH的病理改变,是研究梗阻性PAH的最佳动物模型. PDE1C在PAH动物模型肺动脉平滑肌细胞中显著上调,可能成为肺动脉高压治疗的新靶点.
目的以左肺切除(PE)+野百閤堿(MCT)建立大鼠肺動脈高壓(PAH)新生內膜模型,探討燐痠二酯酶1C(PDE1C)在該模型肺組織中的錶達水平及作用.方法採用單純PE、MCT、PE+MCT(P+M)3種方法建立大鼠PAH模型;檢測模型大鼠平均肺動脈壓力(mPAP)、中膜厚度百分比、右心肥厚指數(RV/LV+S)比值,觀察新生內膜形成和非肌性小動脈肌化程度,比較3種PAH動物模型肺血管重構模式的差異;採用免疫組化檢測PDE1C在3種動物模型肺組織中的錶達水平.結果P+M組右肺腺泡內血管齣現新生內膜病變,且動物齣現嚴重右心室肥大,肺動脈中膜增厚,平均mPAP和無肌性血管肌化程度較其他模型顯著增加.大鼠PAH新生內膜模型PDE1C蛋白錶達顯著增加(P<0.05).結論P+M模型能更好地模擬人類嚴重PAH的病理改變,是研究梗阻性PAH的最佳動物模型. PDE1C在PAH動物模型肺動脈平滑肌細胞中顯著上調,可能成為肺動脈高壓治療的新靶點.
목적이좌폐절제(PE)+야백합감(MCT)건립대서폐동맥고압(PAH)신생내막모형,탐토린산이지매1C(PDE1C)재해모형폐조직중적표체수평급작용.방법채용단순PE、MCT、PE+MCT(P+M)3충방법건립대서PAH모형;검측모형대서평균폐동맥압력(mPAP)、중막후도백분비、우심비후지수(RV/LV+S)비치,관찰신생내막형성화비기성소동맥기화정도,비교3충PAH동물모형폐혈관중구모식적차이;채용면역조화검측PDE1C재3충동물모형폐조직중적표체수평.결과P+M조우폐선포내혈관출현신생내막병변,차동물출현엄중우심실비대,폐동맥중막증후,평균mPAP화무기성혈관기화정도교기타모형현저증가.대서PAH신생내막모형PDE1C단백표체현저증가(P<0.05).결론P+M모형능경호지모의인류엄중PAH적병리개변,시연구경조성PAH적최가동물모형. PDE1C재PAH동물모형폐동맥평활기세포중현저상조,가능성위폐동맥고압치료적신파점.
@@@@Objective To establish a neointima model of pulmonary arterial hypertension (PAH) in rats by pneumonectomy(PE) and monoerotatine(MCT),and to investigate the expression and function of phosphodiesterase 1C (PDE1C) protein in this PAH model.Methods Three approaches were used to establish PAH model in rats:left lung PE group(PE group),MCT injection group,and MCT injection after PE group (P+M group).Mean pulmonary arterial pressure(mPAP),percentage of media thickness(MT%) and the ratio of right ventricular hypertrophy index (RV/LV+S) of model rats were recorded.Morphological parameters relevant to neointima formation and the muscularization of nonmuscle pulmonary arterioles were observed,and the difference of pulmonary vascular remodeling pattern of the three PAH models was analyzed.The expression of PDE1C was detected in each group by immunohistochemitry.Results The P+M group showed serious lesions in the neointim and right ventricular,and serious right ventricular hypertrophy,and the increasing MT of pulmonary arterials could be seen in the animals.Compared with other groups,P+M group had a significantly higher mPAP and muscularization of nonmuscle arterioles developed significantly.Expression of PDE1C protein increased significantly in the neointima PAH model(P<0.05).Conclusion P+M model is a good model for simulation of severe PAH in human , which is the best animal model for a study on the obstructive PAH.Up-regulation of PDE1C in pulmonary artery smooth muscle cells of PAH animal model might offer a new target for therapy of PAH in human .