内皮舒张因子和内皮素之间调控关系动物实验研究  

Animal Experimental Study between the EDRF/NO And Endothelin in Regulative Relations

作　　者：孙奥丽[1] 孙永波[1] 孙海峰[1,2] 陈红霞[1] 

机构地区：[1]山东省淄博科技职业学院生理,药理室,255015 [2]山东大学南区校医院

出　　处：《医学研究杂志》2007年第3期61-63,共3页Journal of Medical Research

摘　　要：目的探讨内皮舒张因子(EDRF/NO)和内皮素(endothelin,ET)之间的调控关系。方法在设置整体和离体大鼠主动脉灌流模型上,进行相关因素灌流,观察平均动脉压(MABP)、血浆ET水平、组织环一磷酸鸟苷(cGMP)含量的动态变化。结果整体实验结果:①ET组MABP先瞬时(1～2min)降低6.58±0.67kPa,随后进行性升高,呈双向反应,达30min时MABP较给药前升高33.3±0.4kPa;主动脉的cGMP含量升高,较对照组增加74.5%;②L-NNA组MABP缓慢上升,30min时升高至4.62±2.04kPa;cGMP水平较对照组减少5倍(0.42±0.08vs2.14±0.18pmol/mgPr,P<0.01),而血浆ET-ir升高[(819±60pg/(g.w.w)vs对照组514±50pg/(g.w.w),P<0.01];③L-NNA+ET组,实验30min时,MABP升高至6.49±3.6kPa;较L-NNA组cGMP含量无明显增加(P>0.05);④Ach灌流,血管ET释放减少[406±31vs对照组514±50pg/(g.w.w),P<0.01]。离体灌流实验结果:①ET灌流不能使去内皮的血管cGMP含量升高(0.27±0.04vs对照组0.24±0.06pmol/mgPr);②MB灌流,使cGMP含量升高(0.64±0.07vs对照组214±0.18pmol/mgPr,P<0.01),但不影响ET释放。结论ET可能通过自分泌方式促使EC释放EDRF/NO,EDRF/NO既拮抗ET的生物学效应,又对ET起着负反馈调节作用。Objective To probe into modulation effect between the EDRF/NO And ET. Methods In the whole Wister rat and rat＇s aorta perfusion model ,they are carried through relative factors so that dynamic change of MABP , plasm ET - ir and cGMP level of tissue is observed. Besults Whole Wister rat＇s experiment results ： ① In ET group, MABP first instantly（ 1 ～ 2min） reduces 6.58 ± 0.67kPa, afterwards duratively enhances ,it assumes the bidirectional response, when it reaches to 30min, MABP elevates 33.3 ± 0.4kPa than before taking ET;Canses the aortic cGMP content to elevate, comparatively group control to increase 74.5% ; ② In L - NNA group ,MABP slow rise, within 30min elevates to 4.62 ± 2.04kPa; With control group comparison , the GMP level is reduced 5 times （0.42 ± 0.08 versus the control 2.14 e0.18pmol/mg Pr,P 〈0.01 ）. But blood plasma ET- ir enhances E819 e60pg/（ g. w. w） versus control group 514 ± 50pg/（ g. w. w） ,P 〈0.01 ] ;③ In the L- NNA ＋ ET group, MABP enhances to 6.49 ± 3.6kPa for a period of 30min; Compared with L - NNA, the cGMP content is not too obviously increases （ P 〉 0.05 ） ; ④ In Ach group, The vascular ET release reduces E 406 ± 31 versus control group 514 ± 50pg/（ g. w. w） , P 〈 0.01 ]. Experiment results of aorta perfusion model ： ① ET perfusion cannot cause the removed endothelium vascular cGMP content ascension （0.27 ± 0.04 versus the control group 0.24 e 0.06pmol/mgpr） ;② With MB perfusion, causes cGMP content ascension（0.64 ± 0.07 versus the control 214 ± 0.18pmol/mgpr,P 〈 0.01 ）, but it do not affect release of ET. Conclusions These results susgest that ET promotes EC to release EDBF/NO by autocrine. EDBF/NO may inhibit ET biological effect and also is getting up the negative feedback control action to ET.

关 键 词：内皮舒张因子 内皮素 灌流 调控关系 

分 类 号：R544.102[医药卫生—心血管疾病]