激活PKC降低TAC大鼠肥大心脏的收缩功能  

Activation of protein kinase-C reduces contractile function of hypertrophic heart in transverse aortic constriction rats

作　　者：张蓝宁[1] 张琳[1] 王云英[1] 陈焱[1] 常惠[1] 余志斌[1] 

机构地区：[1]第四军医大学航空航天生理学教研室,陕西西安710032

出　　处：《心脏杂志》2011年第2期184-188,共5页Chinese Heart Journal

基　　金：国家自然科学基金资助课题(30700264)

摘　　要：目的:探究心肌细胞肥大过程中,蛋白激酶C(PKC)激活与心肌收缩功能的关系。方法:用12只雄性SD大鼠原则随机均分为A、B组,A组行腹主动脉缩窄(transverse abdominal aortic constriction,TAC)制备高血压大鼠模型,B组作为对照组,分别术后饲养16周。采用离体工作心脏灌流装置对16周的大鼠心脏进行灌注,同时行左心室内Millar导管插管,监测心功能的各项指标。结果:TAC可引起大鼠的血压显著增高,心肌肥厚,心输出量增多,呈代偿状态。PKC激动剂佛波酯(PMA)可使TAC大鼠的心输出量显著减少,心肌收缩与舒张时间延长,并降低舒张速率。由于收缩与舒张时程延长,舒张速率降低,在高心率下可导致左心室舒张末压抬高,心脏泵血功能大幅降低。结论:PMA可激活16周的TAC大鼠肥大心肌细胞中的PKCs,降低肥大心肌收缩功能,这可能为引起心力衰竭的原因之一。AIM： To observe the effects of protein kinase-C（PKC） on the contractile function of hypertrophic hearts in transverse abdominal aortic constriction（TAC） rats in order to demonstrate whether PKC contributes as a pivotal node during the transition from cardiac hypertrophy to heart failure.METHODS： Twenty-four male Sprague Dawley rats were randomly divided into control and TAC groups.After 16 weeks,the hearts were rapidly removed and working-heart perfusion system and Millar probe were applied to monitor cardiac function.RESULTS： Hypertension,myocardial hypertrophy and an increase in cardiac output were observed in TAC rats.PMA,an agonist to PKC,reduced cardiac output and prolonged the time to peak pressure（TPP） and the time from peak to 75% relaxation（TR75）,resulting in a depression in diastolic rate and inducing a sharp reduction in cardiac output at high heart rates.CONCLUSIONS： PMA activates PKC in hypertrophic hearts of 16-week TAC rats,which may lead to cardiac failure.

关 键 词：蛋白激酶C 佛波酯 主动脉缩窄 心肌肥厚 心力衰竭 大鼠 

分 类 号：Q555.7[生物学—生物化学]