中华结核和呼吸杂志
中華結覈和呼吸雜誌
중화결핵화호흡잡지
Chinese Journal of Tuberculosis and Respiratory Diseases
2008年
1期
37-41
,共5页
张一梅%刘温娟%石玉枝%高宇飞%王丽玲%陈铭新
張一梅%劉溫娟%石玉枝%高宇飛%王麗玲%陳銘新
장일매%류온연%석옥지%고우비%왕려령%진명신
血管紧张素Ⅱ%肺栓塞%高血压,肺性
血管緊張素Ⅱ%肺栓塞%高血壓,肺性
혈관긴장소Ⅱ%폐전새%고혈압,폐성
Urotensin Ⅱ%Pulmonary thromboemblism%Hypertension,pulmonary
目的 研究尾加压素Ⅱ(U Ⅱ)蛋白和mRNA及U Ⅱ受体(UT)mRNA在慢性栓塞性肺动脉高压大鼠肺动脉的表达,探讨其在病程中的作用.方法 雄性Wistar大鼠,麻醉后经颈静脉注入体外制备的血栓栓子,2周后同法进行2次栓塞,造模成功大鼠分为2周组、4周组、8周组、12周组,全程腹腔注射抗纤维溶解剂氨甲环酸,达到目标日期后行以下检查:(1)测量平均肺动脉压(mPAP);(2)用免疫学检验和原位杂交的方法检测不同节段肺动脉U Ⅱ蛋白和mRNA表达及UT mRNA表达;(3)在光镜下观察肺动脉显微结构的变化,测定肺动脉相对中膜厚度(PAMT)和管壁面积/管总面积(WA/TA).采用SPSS 13.0软件,所有数据以-x±s表示,组间比较采用单因素方差分析,组间差异采用LSD方差分析.结果 (1)栓塞后4、8及12周组的大鼠mPAP值分别为(19.9±6.2)mm Hg(1 mm Hg=0.133 kPa)、(23.8±4.1)mm Hg、(27.4±5.4)mm Hg,较对照组明显升高(F值为13.75,P＜0.01),PAMT百分比分别为42.6±11.16、47.82±10.02、53.79±10.41,WA/TA百分比分别为22.75±6.79、25.32±4.90、27.05±7.71,较对照组均明显增大(F值分别为5.52和6.61,P均＜0.01);(2)栓塞后肺动脉U Ⅱ蛋白和U Ⅱ mRNA以及UT mRNA表达上调,细小动脉较中型动脉变化更为明显,4、8及12周组肺细小动脉U Ⅱ mRNA和UT mRNA及U Ⅱ蛋白平均吸光度值分别为0.138±0.019、0.144±0.022、0.173±0.021和0.126±0.028、0.146±0.029、0.157±0.025,与对照组相比明显升高(F值分别为30.39、30.78和14.49,P均＜0.01),随着栓塞时间的延长,表达呈明显增加的趋势;(3)肺细小动脉U Ⅱ蛋白和mRNA及UT mRNA的平均吸光度值均与mPAP、PAMT呈正相关关系(r值分别为0.822、0.866、0.846;0.675、0.712、0.756,P均＜0.01).结论 慢性栓塞性肺动脉高压大鼠出现明显肺动脉重构,尾加压素Ⅱ蛋白和mRNA及其UT mRNA在肺动脉表达明显上调,其动态变化与肺动脉高压、肺血管重构的病理过程明显相关.
目的 研究尾加壓素Ⅱ(U Ⅱ)蛋白和mRNA及U Ⅱ受體(UT)mRNA在慢性栓塞性肺動脈高壓大鼠肺動脈的錶達,探討其在病程中的作用.方法 雄性Wistar大鼠,痳醉後經頸靜脈註入體外製備的血栓栓子,2週後同法進行2次栓塞,造模成功大鼠分為2週組、4週組、8週組、12週組,全程腹腔註射抗纖維溶解劑氨甲環痠,達到目標日期後行以下檢查:(1)測量平均肺動脈壓(mPAP);(2)用免疫學檢驗和原位雜交的方法檢測不同節段肺動脈U Ⅱ蛋白和mRNA錶達及UT mRNA錶達;(3)在光鏡下觀察肺動脈顯微結構的變化,測定肺動脈相對中膜厚度(PAMT)和管壁麵積/管總麵積(WA/TA).採用SPSS 13.0軟件,所有數據以-x±s錶示,組間比較採用單因素方差分析,組間差異採用LSD方差分析.結果 (1)栓塞後4、8及12週組的大鼠mPAP值分彆為(19.9±6.2)mm Hg(1 mm Hg=0.133 kPa)、(23.8±4.1)mm Hg、(27.4±5.4)mm Hg,較對照組明顯升高(F值為13.75,P＜0.01),PAMT百分比分彆為42.6±11.16、47.82±10.02、53.79±10.41,WA/TA百分比分彆為22.75±6.79、25.32±4.90、27.05±7.71,較對照組均明顯增大(F值分彆為5.52和6.61,P均＜0.01);(2)栓塞後肺動脈U Ⅱ蛋白和U Ⅱ mRNA以及UT mRNA錶達上調,細小動脈較中型動脈變化更為明顯,4、8及12週組肺細小動脈U Ⅱ mRNA和UT mRNA及U Ⅱ蛋白平均吸光度值分彆為0.138±0.019、0.144±0.022、0.173±0.021和0.126±0.028、0.146±0.029、0.157±0.025,與對照組相比明顯升高(F值分彆為30.39、30.78和14.49,P均＜0.01),隨著栓塞時間的延長,錶達呈明顯增加的趨勢;(3)肺細小動脈U Ⅱ蛋白和mRNA及UT mRNA的平均吸光度值均與mPAP、PAMT呈正相關關繫(r值分彆為0.822、0.866、0.846;0.675、0.712、0.756,P均＜0.01).結論 慢性栓塞性肺動脈高壓大鼠齣現明顯肺動脈重構,尾加壓素Ⅱ蛋白和mRNA及其UT mRNA在肺動脈錶達明顯上調,其動態變化與肺動脈高壓、肺血管重構的病理過程明顯相關.
목적 연구미가압소Ⅱ(U Ⅱ)단백화mRNA급U Ⅱ수체(UT)mRNA재만성전새성폐동맥고압대서폐동맥적표체,탐토기재병정중적작용.방법 웅성Wistar대서,마취후경경정맥주입체외제비적혈전전자,2주후동법진행2차전새,조모성공대서분위2주조、4주조、8주조、12주조,전정복강주사항섬유용해제안갑배산,체도목표일기후행이하검사:(1)측량평균폐동맥압(mPAP);(2)용면역학검험화원위잡교적방법검측불동절단폐동맥U Ⅱ단백화mRNA표체급UT mRNA표체;(3)재광경하관찰폐동맥현미결구적변화,측정폐동맥상대중막후도(PAMT)화관벽면적/관총면적(WA/TA).채용SPSS 13.0연건,소유수거이-x±s표시,조간비교채용단인소방차분석,조간차이채용LSD방차분석.결과 (1)전새후4、8급12주조적대서mPAP치분별위(19.9±6.2)mm Hg(1 mm Hg=0.133 kPa)、(23.8±4.1)mm Hg、(27.4±5.4)mm Hg,교대조조명현승고(F치위13.75,P＜0.01),PAMT백분비분별위42.6±11.16、47.82±10.02、53.79±10.41,WA/TA백분비분별위22.75±6.79、25.32±4.90、27.05±7.71,교대조조균명현증대(F치분별위5.52화6.61,P균＜0.01);(2)전새후폐동맥U Ⅱ단백화U Ⅱ mRNA이급UT mRNA표체상조,세소동맥교중형동맥변화경위명현,4、8급12주조폐세소동맥U Ⅱ mRNA화UT mRNA급U Ⅱ단백평균흡광도치분별위0.138±0.019、0.144±0.022、0.173±0.021화0.126±0.028、0.146±0.029、0.157±0.025,여대조조상비명현승고(F치분별위30.39、30.78화14.49,P균＜0.01),수착전새시간적연장,표체정명현증가적추세;(3)폐세소동맥U Ⅱ단백화mRNA급UT mRNA적평균흡광도치균여mPAP、PAMT정정상관관계(r치분별위0.822、0.866、0.846;0.675、0.712、0.756,P균＜0.01).결론 만성전새성폐동맥고압대서출현명현폐동맥중구,미가압소Ⅱ단백화mRNA급기UT mRNA재폐동맥표체명현상조,기동태변화여폐동맥고압、폐혈관중구적병리과정명현상관.
Objective To investigate the expressions of Urotensin Ⅱ(U Ⅱ)protein and mRNA and its receptor(UT)mRNA of medium and small pulmonary arteries of rats with chronic thromboembolic pulmonary hypertension. Methods The Wistar rats were injected thrombi through the jugular vein 2 times in 2 weeks and tranexamic acid was injected peritoneally once daily during the experiment to prevent thrombolysis. The mean pulmonary artery pressure(mPAP) was measured using right cardiac atheterzation.The expressions of U Ⅱ protein in pulmonary arteries were studied by immunohischemistry with a polycolonal antibody. The expressions of U Ⅱ mRNA and UT mRNA were detected by in situ hybridization using U Ⅱ and UT oligonuclear probes. The changes of structures in pulmonary vessle were observed,including relative medial thickness of pulmonary artery(PAMT)and vessle wall area/ total vessle area(WA/TA). Results The mPAP of the 4 weeks to the 12 weeks groups were(19.9±6.2)mm Hg(1 mm Hg=0.133 kPa),(23.8±4.1)mm Hg and(27.4±5.4)mm Hg,higher than that of the control group(F=13.75,P＜0.01,respectively).The PAMT of the 4 weeks to the 12 weeks groups were(42.6±11.16)%,(47.82±10.02)% and(53.79±10.41)%, and WA/TA of the 4 weeks to the 12 weeks groups were(22.75±6.79)%,(25.32±4.90)%and(27.05±7.71)%,both changed significantly as compared to the control group(F=5.52 and 6.61,P＜0.01,respectively;P＜0.05 in 4 weeks group;P＜0.01 in 8 weeks and 12 weeks groups,respectively). The expressions of U Ⅱ protein, U Ⅱ mRNA and UT mRNA in the 4 weeks to the 12 weeks groups were obviously higher than the control group(F=30.39,30.78 and 14.49,P＜0.01,respectively), and their expressions were more marked in the small pulmonary arteries than in medium pulmonary arteries. The expressions of U Ⅱ protein,U Ⅱ mRNA and UT mRNA were positively correlated with mPAP and PAMT. The pulmonary vascular remodeling was time-dependently aggravated after embolism(r:0.822,0.866 and 0.846;0.675,0.712 and 0.756,P＜0.01,respectively). Conclusions The expressions of U Ⅱ protein. U Ⅱ mRNA and UT mRNA of pulmonary arteries in the animal models were higher than those in the control group. These dynamic changes of U Ⅱ mRNA,U Ⅱ protein and UT mRNA may contribute to the development of pulmonary hypertension and vascular remodeling after pulmonary thromboembolism.
