中华实验外科杂志
中華實驗外科雜誌
중화실험외과잡지
CHINESE JOURNAL OF EXPERIMENTAL SURGERY
2015年
5期
1081-1083
,共3页
钙离子%肺叶切除%野百合碱
鈣離子%肺葉切除%野百閤堿
개리자%폐협절제%야백합감
Ca2+%Pneumonectomy%Monocrotaline
目的 探讨规范性瞬时感受器电位通道1(TRPC1)蛋白-钙池操纵性钙通道(SOCC)在新型肺高压发病过程中的作用.方法 在左肺叶切除(PE)复合腹腔注射野百合碱(MCT)的肺高压大鼠模型中观察SOCC表达及功能变化.结果 与对照组(CON)比较,PE+ MCT组TRPC1mRNA为其(3.40±1.59)倍(P＜0.05);环匹阿尼酸(CPA)触发的肺动脉收缩由(16.6±1.5)％增加至(126.6±15.4)％(P＜0.01),肺动脉平滑肌细胞的[Ca2+]i由(268±76) nmol/L增加至(1 832±867) nmol/L(P ＜0.01);钆离子舒张效应由(36.9±3.7)％增加至(70.1±2.6)％(P＜0.05).结论 PE+ MCT上调了大鼠肺动脉TRPC1表达,增强了由TRPC1/SOCC介导的肺动脉平滑肌细胞的Ca2+内流和肺血管收缩,从而诱导大鼠产生肺高压,并进一步诱发肺血管及右心室重构.
目的 探討規範性瞬時感受器電位通道1(TRPC1)蛋白-鈣池操縱性鈣通道(SOCC)在新型肺高壓髮病過程中的作用.方法 在左肺葉切除(PE)複閤腹腔註射野百閤堿(MCT)的肺高壓大鼠模型中觀察SOCC錶達及功能變化.結果 與對照組(CON)比較,PE+ MCT組TRPC1mRNA為其(3.40±1.59)倍(P＜0.05);環匹阿尼痠(CPA)觸髮的肺動脈收縮由(16.6±1.5)％增加至(126.6±15.4)％(P＜0.01),肺動脈平滑肌細胞的[Ca2+]i由(268±76) nmol/L增加至(1 832±867) nmol/L(P ＜0.01);釓離子舒張效應由(36.9±3.7)％增加至(70.1±2.6)％(P＜0.05).結論 PE+ MCT上調瞭大鼠肺動脈TRPC1錶達,增彊瞭由TRPC1/SOCC介導的肺動脈平滑肌細胞的Ca2+內流和肺血管收縮,從而誘導大鼠產生肺高壓,併進一步誘髮肺血管及右心室重構.
목적 탐토규범성순시감수기전위통도1(TRPC1)단백-개지조종성개통도(SOCC)재신형폐고압발병과정중적작용.방법 재좌폐협절제(PE)복합복강주사야백합감(MCT)적폐고압대서모형중관찰SOCC표체급공능변화.결과 여대조조(CON)비교,PE+ MCT조TRPC1mRNA위기(3.40±1.59)배(P＜0.05);배필아니산(CPA)촉발적폐동맥수축유(16.6±1.5)％증가지(126.6±15.4)％(P＜0.01),폐동맥평활기세포적[Ca2+]i유(268±76) nmol/L증가지(1 832±867) nmol/L(P ＜0.01);구리자서장효응유(36.9±3.7)％증가지(70.1±2.6)％(P＜0.05).결론 PE+ MCT상조료대서폐동맥TRPC1표체,증강료유TRPC1/SOCC개도적폐동맥평활기세포적Ca2+내류화폐혈관수축,종이유도대서산생폐고압,병진일보유발폐혈관급우심실중구.
Objective To investigate the role of canonical transient receptor potential 1 (TRPC1)in pneumonectomy (PE) plus subcutaneous injection of monocrotaline (MCT)-induced pulmonary artery hypertension (PH) in rats.Methods SD rats underwent unilateral lobectomy,and 1 week later,rats were intraperitoneally injected with 2％ MCT (50 mg/kg).After 3 weeks,mean right ventricular pressure (mRVP) and right ventricular mass index (RVMI) were measured.The lung sections were stained by hematoxylin and eosin (HE) and observed under light microscope.Real-time reverse transcriptase-polymerase chain reaction(RT-qPCR) was performed to detect TRPC1 mRNA expression in rat pulmonary arteries (PAs).Store-operated calcium channel (SOCC) agonist cyclopiazonic acid (CPA)-induced PAs contraction was measured by vascular ring tension analysis and the intracellular Ca2+ concentration ([Ca2 +] i) of pulmonary artery smooth muscle cells (PASMCs) was monitored by Fluo3-AM assay.Meanwhile the effect of endothelin-1 (ET-1)-induced vasocontration,and the relaxation of gadolinium (Gd3 +) on ET-1-induced PAs contraction was measured.Results In comparison to the control group,rats developed severe PAH,and right ventricular hypertrophy in PE + MCT group.The expression of TRPC1 mRNA in control group was more than 3 folds of that in PE + MCT group.CPA-induced vasoconstriction was increased from (16.6 ± 1.5)％ in control group to (126.6 ± 15.4)％ in PE + MCT group (n =8,P ＜ 0.01),and Ca2 + influx in PASMCs evoked by CPA was enhanced from (268 ± 76) nmol/L in control group to (1 832 ± 867) nmol/L in PE + MCT group (n =8,P ＜ 0.01).Gd3 +-induced relaxation to Endothelin-1 vasoconstriction was also potentiated from (36.9 ± 3.7) ％ in control group to (70.1 ±2.6) ％ in PE + MCT group (n =8,P ＜ 0.05).Conclusion PE + MCT-induced PH is associated with increased TRPC1 expression and TRPC/SOCC-induced store operated Ca2 + entry.
