Arterial baroreflex buffering of sympathetic activation during exercise-induced elevations in arterial pressure.
Arterial baroreflex buffering of sympathetic activation during exercise-induced elevations in arterial pressure.
复制标题
在运动引起的动脉压升高期间，动脉压力反射缓冲交感神经激活。
DOI：
10.1172/jci114916
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发表时间：
1990
期刊：
影响因子：
--
通讯作者：
Victor,RG
中科院分区：
文献类型：
--
作者：
Scherrer,U;Pryor,SL;Bertocci,LA;Victor,RG
静态肌肉收缩会激活代谢敏感的肌肉传入神经，从而反射性地增加交感神经活动和动脉压。为了确定这种收缩诱导的反射是否受到窦主动脉压力反射的调制，我们进行了交感神经活动的微电极记录，以休息腿部肌肉在人类静态握力，同时试图通过控制运动引起的血压升高与药理学药物钳位压力反射刺激的水平。主要的新发现是，部分药物抑制在静态握力（硝普钠输注）的血压升高增加运动引起的心率和交感神经活动增加了300%以上。运动引起的血压升高的药理学加重（苯肾上腺素输注）使这些反射增加减弱了50%以上。与此相反，这些药物操作在动脉压有很少或没有影响：（a）前臂肌细胞pH值，骨骼肌传入的代谢刺激的指数;或（B）中心静脉压，心肺传入的机械刺激的指数。我们的结论是，在人类的窦主动脉压力感受器反射是更有效的缓冲静态肌肉收缩引起的反射交感神经激活比以前认为的。
Static muscle contraction activates metabolically sensitive muscle afferents that reflexively increase sympathetic nerve activity and arterial pressure. To determine if this contraction-induced reflex is modulated by the sinoaortic baroreflex, we performed microelectrode recordings of sympathetic nerve activity to resting leg muscle during static handgrip in humans while attempting to clamp the level of baroreflex stimulation by controlling the exercise-induced rise in blood pressure with pharmacologic agents. The principal new finding is that partial pharmacologic suppression of the rise in blood pressure during static handgrip (nitroprusside infusion) augmented the exercise-induced increases in heart rate and sympathetic activity by greater than 300%. Pharmacologic accentuation of the exercise-induced rise in blood pressure (phenylephrine infusion) attenuated these reflex increases by greater than 50%. In contrast, these pharmacologic manipulations in arterial pressure had little or no effect on: (a) forearm muscle cell pH, an index of the metabolic stimulus to skeletal muscle afferents; or (b) central venous pressure, an index of the mechanical stimulus to cardiopulmonary afferents. We conclude that in humans the sinoaortic baroreflex is much more effective than previously thought in buffering the reflex sympathetic activation caused by static muscle contraction.