慢性低氧和野百合碱预处理上调大鼠肺动脉平滑肌细胞静息Ca^(2+)内流

Chronic Hypoxia and Monocrotaline Pretreatment Increases the Resting Cacium Entry of Pulmonary Artery Smooth Muscle Cells in Rats

目的探讨慢性低氧(CH)和野百合碱(MCT)预处理对于大鼠肺动脉平滑肌细胞(PASMCs)静息Ca2+内流的影响。方法持续低氧暴露或一次性腹腔注射野百合碱构建肺高压大鼠模型;酶消化法分离大鼠PASMCs,然后进行α-肌动蛋白(α-Actin)细胞免疫化学鉴定;采用锰(Mn2+)淬灭实验测定PASMCs静息Ca2+内流。结果肺高压大鼠模型构建成功;光镜下PASMCs为长梭形,呈典型的"峰-谷"状生长,免疫化学α-Actin鉴定显示,绝大部分PASMCs胞质呈棕褐色;CH和MCT组PASMCs基础Mn2+淬灭速率和幅度均显著增加。结论 CH和MCT预处理均能上调大鼠PASMCs静息Ca2+内流。

Objective To investigate the effects of chronic hypoxia （CH） and monocrotalim （MCT） on the resting [Ca2＋]i of pulmonary arterial smooth muscle cells. Method We employed 2 t）ro cedures to induce thePH rat models, i.e. exposed to a long period of hypoxia and administration of mono crotaline hydrochloride in rats. Rat PASMCs were enzymatically isolated, α-smooth muscle actin（α-SM actin） within the ceils was identified through immunohistochemistry. We observed Ca2. influx of pulmonary arterial smooth muscle cells by the means of Mn2＋ quenching. Results The two PH models were established successfully. The cells tended to be long spindle and grew in the ＂peak-valley＂ mode under light microscope, immunology results showed that most endochylema were stained in brownish yellow. The resting rate and magnitude of Mn2＋ quenching in pre-treated（CH and MCT） PASMCs were respec- tively increased. Conclusions Chronic hypoxia and monocrotaline pretreated increases the resting [Ca2＋ ]i of rat pulmonary artery smooth muscle cells.