Muscle chemoreflex-induced increases in right atrial pressure.
Muscle chemoreflex-induced increases in right atrial pressure.
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肌肉化学反射引起右心房压力增加。
DOI：
10.1152/ajpheart.1998.275.3.h767
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发表时间：
1998
期刊：
影响因子：
--
通讯作者：
O'Leary,DS
中科院分区：
文献类型：
--
作者：
Sheriff,DD;Augustyniak,RA;O'Leary,DS
当输送到活动肌肉的氧气对于正在进行的代谢速率来说太低时，代谢物积累并刺激肌肉内的感觉神经，导致交感神经激活（肌肉化学反射）。迄今为止，对这种反射的研究主要集中在其增加动脉压的能力或介导这种反应的神经的活动上。显然，心输出量（CO）的增加构成了一种重要的调节，因为它增加了可用于分配在竞争流动的器官之间的总血流量。然而，心率和收缩性的增加提供了有限的提高CO的手段，因为在完整循环中CO和右心房压力（RAP）之间存在反比关系。我们的目标是测试肌肉化学反射激活，通过部分血管闭塞，后肢血流量的分级减少，elevenness外周血管的调整，提高RAP。在四个清醒的狗在跑步机上行使在3.2公里/小时0%的等级，RAP保持良好的反射激活期间，尽管增加CO和动脉压，预计减少RAP。因此，由反射引起的外周血管调节成功地保护了RAP，否则它会下降。为了分离反射对RAP的影响，通过心室起搏结合阿替洛尔β1-肾上腺素能阻滞来维持CO恒定。当通过将后肢血流量从0.6 l/min减少到0.3 l/min来激活反射时，RAP从5.1 ± 0.8上升到7.4 ± 0.4 mmHg（P< 0.05），尽管动脉压持续大幅增加（40 mmHg）。5条心功能正常的犬在较重的运动（6.4km/h 10%）中，尽管CO和动脉压增加，RAP反射仍从5.7 ± 0.9上升到6.6 ± 0.8mmHg（P< 0.05）。我们的结论是，肌肉化学反射能够引起RAP的大幅增加。
When oxygen delivery to active muscle is too low for the ongoing rate of metabolism, metabolites accumulate and stimulate sensory nerves within the muscle leading to sympathetic activation (muscle chemoreflex). To date, studies on this reflex have focused primarily on its ability to increase arterial pressure or on the activity of the nerves that mediate this response. Clearly, a rise in cardiac output (CO) constitutes an important adjustment, because it increases the total blood flow available to be distributed among organs competing for flow. However, increments in heart rate and contractility provide limited means of raising CO because of the inverse relationship that exists between CO and right atrial pressure (RAP) in the intact circulation. Our goal was to test whether muscle chemoreflex activation, achieved via graded reductions in hindlimb blood flow by partial vascular occlusion, elicits peripheral vascular adjustments that raise RAP. In four conscious dogs exercising on a treadmill at 3.2 km/h 0% grade, RAP was well maintained during reflex activation despite increases in CO and arterial pressure that are expected to reduce RAP. Thus peripheral vascular adjustments elicited by the reflex successfully defend RAP in a setting where it would otherwise fall. To isolate the effects of the reflex on RAP, CO was maintained constant by ventricular pacing in conjunction with β1-adrenergic blockade with atenolol. When the reflex was activated by reducing hindlimb blood flow from 0.6 to 0.3 l/min, RAP rose from 5.1 ± 0.8 to 7.4 ± 0.4 mmHg (P< 0.05) despite continued large (40 mmHg) increases in arterial pressure. During heavier exercise (6.4 km/h 10% grade) in five dogs with normal ventricular function, the reflex raised RAP from 5.7 ± 0.9 to 6.6 ± 0.8 mmHg (P< 0.05) despite increases in CO and arterial pressure. We conclude that the muscle chemoreflex is capable of eliciting substantial increases in RAP.
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