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首页> 外文期刊>American Journal of Physiology >Rapid resetting of carotid baroreceptor reflex by afferent input from skeletal muscle receptors.
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Rapid resetting of carotid baroreceptor reflex by afferent input from skeletal muscle receptors.

机译:通过骨骼肌受体的传入输入快速复位颈动脉压力感受器反射。

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Resetting of the arterial baroreflex is mediated by central (central command) or peripheral (exercise pressor reflex) mechanisms. The purpose of this study was to determine the effect of somatosensory input from skeletal muscle receptors on resetting of the carotid baroreceptor reflex. Resetting of the baroreflex was determined by measuring carotid sinus threshold pressure (Pth) during a ramp protocol that consisted of a linear increase in sinus pressure from 50 to 250 mmHg at approximately 3 mmHg/s. Experiments were performed in seven alpha-chloralose-anesthetized and vagotomized dogs. To determine the effect of skeletal muscle afferent input on resetting, electrically induced muscle contraction was used to activate mechanically and metabolically senstive afferent fibers, whereas passive stretch of the hindlimb was used to activate predominantly mechanically sensitive afferent fibers. Pth for heart rate (HR) and arterial blood pressure (BP) during the control ramp protocol was 110 +/- 4 and 118 +/- 7 mmHg, respectively. Electrically induced muscle contraction increased hindlimb tension (5.7 +/- 0.4 kg) and significantly increased Pth-HR and Pth-BP above control (135 +/- 6 and 141 +/- 5 mmHg, respectively; P < 0.05). Muscle paralysis prevented the increase in Pth-HR and Pth-BP during ventral root stimulation (104 +/- 7 and 116 +/- 5 mmHg, respectively; P = not significant). Passive muscle stretch (n = 3) increased hindlimb tension (5.9 +/- 0.9 kg) and significantly increased Pth-BP (125 +/- 21 vs. 159 +/- 16 mmHg, control vs. contraction; P < 0.05). There was no difference in the magnitude of Pth resetting between muscle contraction or stretch. The present study demonstrates that activation of skeletal muscle afferent fibers, by either muscle contraction or stretch, increases Pth of the carotid baroreflex. Therefore, neural input from skeletal muscle receptors resets the carotid baroreflex in a manner similar to that ascribed by central command.
机译:动脉压力反射的复位是由中央(中央命令)或周围(运动加压反射)机制介导的。这项研究的目的是确定骨骼肌受体的体感输入对复位颈动脉压力感受器反射的影响。压力反射的复位是通过在斜坡方案中测量颈动脉窦阈值压力(Pth)来确定的,该过程包括以大约3 mmHg / s的速度从50 mmHg线性增加到250 mmHg。实验是在七只经α-氯醛糖麻醉和迷走神经的狗中进行的。为了确定骨骼肌传入输入对复位的影响,电诱导的肌肉收缩被用来激活机械和代谢敏感的传入纤维,而后肢的被动拉伸被用来激活主要是机械敏感的传入纤维。在控制斜坡方案期间,心率(HR)和动脉血压(BP)的Pth分别为110 +/- 4和118 +/- 7 mmHg。电引起的肌肉收缩增加后肢张力(5.7 +/- 0.4 kg),并显着增加Pth-HR和Pth-BP高于对照(分别为135 +/- 6和141 +/- 5 mmHg; P <0.05)。肌肉麻痹阻止了腹侧根刺激过程中Pth-HR和Pth-BP的升高(分别为104 +/- 7和116 +/- 5 mmHg; P =不显着)。被动肌肉拉伸(n = 3)增加后肢张力(5.9 +/- 0.9 kg),并显着增加Pth-BP(125 +/- 21 vs. 159 +/- 16 mmHg,对照vs.收缩; P <0.05)。肌肉收缩或伸展之间的Pth复位幅度没有差异。本研究表明,通过肌肉收缩或拉伸引起的骨骼肌传入纤维的激活会增加颈动脉压力反射的Pth。因此,来自骨骼肌受体的神经输入以类似于中央命令的方式复位颈动脉压力反射。

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