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目的探讨环孢素A(cyclosporine A,CsA)是否逆转野百合碱(monocrotaline,MCT)诱导的右心室重构及其作用机制的初步探讨。方法雄性SD大鼠随机分正常对照组,MCT模型组,CsA低、高剂量组(0.33和1mg·kg-1)。MCT造模后14～21d给CsA(ig,bid)。造模22d右心导管术检测右室收缩压(RVSP);称右室自由壁(RV)及左心室加室间隔(LV+SEP)重,计算右心肥大指数(RVHI=RV/LV+SEP);光镜及电镜观察右室结构变化;免疫组化检查右室心肌细胞PCNA的表达。结果CsA逆转MCT所引起RVSP、RVHI的升高(P<0.05或P<0.01)、右室心肌细胞肥大、线粒体肿胀变性及PCNA抗原的过表达。高剂量CsA作用更明显。结论CsA(1mg·kg-1ig,bid)能明显逆转MCT诱导的右室重构,其机制可能与降低右室后负荷及抑制右室心肌细胞肥大有关。
Objective To investigate whether cyclosporine A (CsA) reverses right ventricular remodeling induced by monocrotaline (MCT) and its possible mechanism. Methods Male SD rats were randomly divided into normal control group, MCT model group, CsA low and high dose groups (0.33 and 1 mg · kg -1). CsA (ig, bid) was administered 14 to 21 days after MCT modeling. The right ventricular systolic pressure (RVSP) was measured by right ventricular catheterization at 22 days after modeling. Right ventricular hypertrophy index (RVHI = RV / LV + SEP) was calculated as RV RV and LV + SEP. ). The changes of the right ventricular structure were observed under light microscope and electron microscope. The expression of PCNA in right ventricular myocytes was detected by immunohistochemistry. Results CsA reversed the increase of RVSP and RVHI induced by MCT (P <0.05 or P <0.01), hypertrophy of right ventricular myocardium, swelling and degeneration of mitochondria and over-expression of PCNA antigen. High-dose CsA effect is more obvious. Conclusions CsA (1 mg · kg-1, bid) can obviously reverse the remodeling of right ventricle induced by MCT. The mechanism may be related to reducing the post-right ventricular load and inhibiting the hypertrophy of right ventricular myocardium.