陕西医学杂志
陝西醫學雜誌
협서의학잡지
SHAANXI MEDICAL JOURNAL
2015年
1期
12-14,72
,共4页
高血压, 肺性/化学诱导%微粒体/代谢%一氧化氮合酶/代谢%弹性蛋白/代谢%模型,动物%大鼠
高血壓, 肺性/化學誘導%微粒體/代謝%一氧化氮閤酶/代謝%彈性蛋白/代謝%模型,動物%大鼠
고혈압, 폐성/화학유도%미립체/대사%일양화담합매/대사%탄성단백/대사%모형,동물%대서
Hypertension,pulmonary/chemically induced%Micromes/metabolism%Nitric-oxide synthase/metabolism%Elastin/metabolism%Model,animal%Rats
目的：研究循环微粒（MPs）在肺动脉高压（PH）大鼠体内含量的改变及其与肺动脉高压的关系。方法：将48只雄性 Wistar大鼠中30只随机分为对照组、MCT3组（M3组）、MCT5组（M5组）3组，每组10只。M3组、M5组用野百合碱一次性腹腔注射诱导PH模型，剩余的18只用于后续血管环检测。M3组和M5组分别在注射野百合碱后3周（中期）和5周（晚期）时右心导管法测定右心室收缩压（RVSP）来间接反映肺动脉压力，然后用腹主动脉采血法抽取大鼠血液并提取和检测MPs。用提取的三组MPs刺激大鼠肺动脉（每组6只）后检测内皮型一氧化氮合酶（eNOS）、弹性蛋白（elastin）蛋白的变化。结果：大鼠血浆MPs 含量随PH病情进展而逐渐升高（M5＞ M3＞C）；MPs处理肺动脉后可下调eNOS表达，但是上调elastin表达，而且这一作用与PH病情相关，即M5作用强于M3（P＜0．05）。结论：MPs随PH进展逐渐升高，升高的MPs可以损害内皮功能，这一发现进一步完善了PH的发病机制，为将来防治PH提供理论依据。
目的：研究循環微粒（MPs）在肺動脈高壓（PH）大鼠體內含量的改變及其與肺動脈高壓的關繫。方法：將48隻雄性 Wistar大鼠中30隻隨機分為對照組、MCT3組（M3組）、MCT5組（M5組）3組，每組10隻。M3組、M5組用野百閤堿一次性腹腔註射誘導PH模型，剩餘的18隻用于後續血管環檢測。M3組和M5組分彆在註射野百閤堿後3週（中期）和5週（晚期）時右心導管法測定右心室收縮壓（RVSP）來間接反映肺動脈壓力，然後用腹主動脈採血法抽取大鼠血液併提取和檢測MPs。用提取的三組MPs刺激大鼠肺動脈（每組6隻）後檢測內皮型一氧化氮閤酶（eNOS）、彈性蛋白（elastin）蛋白的變化。結果：大鼠血漿MPs 含量隨PH病情進展而逐漸升高（M5＞ M3＞C）；MPs處理肺動脈後可下調eNOS錶達，但是上調elastin錶達，而且這一作用與PH病情相關，即M5作用彊于M3（P＜0．05）。結論：MPs隨PH進展逐漸升高，升高的MPs可以損害內皮功能，這一髮現進一步完善瞭PH的髮病機製，為將來防治PH提供理論依據。
목적：연구순배미립（MPs）재폐동맥고압（PH）대서체내함량적개변급기여폐동맥고압적관계。방법：장48지웅성 Wistar대서중30지수궤분위대조조、MCT3조（M3조）、MCT5조（M5조）3조，매조10지。M3조、M5조용야백합감일차성복강주사유도PH모형，잉여적18지용우후속혈관배검측。M3조화M5조분별재주사야백합감후3주（중기）화5주（만기）시우심도관법측정우심실수축압（RVSP）래간접반영폐동맥압력，연후용복주동맥채혈법추취대서혈액병제취화검측MPs。용제취적삼조MPs자격대서폐동맥（매조6지）후검측내피형일양화담합매（eNOS）、탄성단백（elastin）단백적변화。결과：대서혈장MPs 함량수PH병정진전이축점승고（M5＞ M3＞C）；MPs처리폐동맥후가하조eNOS표체，단시상조elastin표체，이차저일작용여PH병정상관，즉M5작용강우M3（P＜0．05）。결론：MPs수PH진전축점승고，승고적MPs가이손해내피공능，저일발현진일보완선료PH적발병궤제，위장래방치PH제공이론의거。
Objective:To investigate change of circulating microparticles (MPs) in pulmonary hyperten‐sion rats and its relationship with pulmonary hypertension. Methods:48 healthy male Wistar rats were randomly di‐vided into three groups. All rats except those in control group were injected intraperitoneally (ip) with a single dose (50 mg/kg) of MCT to induce PH. Right ventricular systolic pressure (RVSP) was measured at 3 and 5 weeks be‐fore extracting rat blood from abdominal aortic for MPs detecting. Rat pulmonary artery (n= 6) were stimulated with the extracted MPs, changes of endothelial nitric oxide synthase (eNOS), elastin were detected. Results :Plas‐ma MPs level in rats increased gradually with PH disease progression (M5 > M3 >C);MPs down‐regulate eNOS, but up‐regulate elastin expression in rat pulmonary artery, and this effect was related with PH progression. Conclu‐sion :Plasma MPs level in rats increased gradually with PH disease progression, the increased MPs can impair endo‐thelial function, this finding further perfects the mechanism of PH, and provide a theoretical basis for the future pre‐vention and treatment of PH.
