Role of the exercise pressor reflex in rats with dilated cardiomyopathy.
Role of the exercise pressor reflex in rats with dilated cardiomyopathy.
复制标题
运动升压反射在扩张型心肌病大鼠中的作用。
DOI：
10.1161/01.cir.0000084538.40542.56
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发表时间：
2003
期刊：
影响因子：
--
通讯作者：
Garry,MaryG
中科院分区：
文献类型：
--
作者：
Smith,ScottA;Mammen,PradeepPA;Mitchell,JereH;Garry,MaryG
背景--在心力衰竭中，交感神经介导的运动过动型心血管反应限制了对体力活动的耐受性。骨骼肌形态和代谢的改变导致了运动加压反射(EPR)在心肌病发生后变得过度活跃，并导致了循环反应的夸大。方法和结果：为了验证这一假说，SD大鼠分为对照组、假手术组和扩张型心肌病组(DCM，由缺血损伤诱导)。经胸超声心动图显示对照组、假手术组和DCM组大鼠左室短轴缩短率分别为47±2%、44±1%和24±2%。电诱导的静态肌肉收缩激活EPR导致DCM大鼠平均动脉压和心率的增加(32±2 mm Hg，13±1 bpm)，显著高于对照组(20±1 mm Hg，8±1 bpm)和假手术组(20±2 mm Hg，8±1 bpm)。通过被动肌肉拉伸选择性刺激EPR的机械敏感部分可获得类似的结果。在10周的时间里，扩张型心肌病的EPR和机械反射活动逐渐增加，并随着左心功能不全程度的增加而增加。结论--在DCM中，对静态肌肉收缩的心血管反应增强部分是由夸大的EPR介导的。肌肉机械反射是导致EPR功能障碍的重要原因。
Background—In heart failure, there is a sympathetically mediated hyperkinetic cardiovascular response to exercise that limits tolerance to physical activity. Alterations in skeletal muscle morphology and metabolism have led to the hypothesis that the exercise pressor reflex (EPR) becomes hyperactive after the development of cardiomyopathy and contributes to the exaggerated circulatory response elicited.Methods and Results—To test this hypothesis, Sprague-Dawley rats were divided into the following groups: control, sham, and dilated cardiomyopathy (DCM, induced by ischemic injury). Using transthoracic echocardiography, left ventricular fractional shortening was 47±2%, 44±1%, and 24±2% in control, sham, and DCM rats, respectively. Activation of the EPR by electrically induced static muscle contraction resulted in significantly larger increases in mean arterial pressure and heart rate in DCM animals (32±2 mm Hg, 13±1 bpm) compared with control (20±1 mm Hg, 8±1 bpm) and sham (20±2 mm Hg, 8±1 bpm) rats. Comparable results were obtained with selective stimulation of the mechanically sensitive component of the EPR by passive muscle stretch. The augmentations in EPR and mechanoreflex activity in DCM occurred progressively over a 10-week period, becoming greater as the severity of left ventricular dysfunction increased.Conclusions—In DCM, the potentiated cardiovascular response to static muscle contraction is mediated, in part, by an exaggerated EPR. The muscle mechanoreflex contributes significantly to the EPR dysfunction that develops.