Alteration of humoral and peripheral vascular responses during graded exercise in heart failure
Alteration of humoral and peripheral vascular responses during graded exercise in heart failure
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DOI：
10.1152/jappl.2001.90.1.55
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发表时间：
2001-01-01
影响因子：
3.3
通讯作者：
O'Leary, DS
中科院分区：
文献类型：
--
作者：
Hammond, RL;Augustyniak, RA;O'Leary, DS
我们假设，在心力衰竭（HF）期间进行运动会导致活动骨骼肌灌注不足，在较低的工作负荷下引起交感神经激活，并改变正常的血流动力学和激素反应。我们测量了心输出量，平均主动脉和右心房压力，后肢和肾血流量（RBF），动脉血浆去甲肾上腺素（NE），血浆肾素活性（PRA），血浆精氨酸加压素（AVP）在7只狗在分级跑台运动和休息。在对照实验中，交感神经激活在较高的工作负荷导致心脏性能的增加，匹配增加的肌肉血管传导。NE、PRA和AVP也增加。运动期间肾血管传导性降低，使得RBF保持在静息水平。对照实验后，通过快速心室起搏诱导HF，并重复运动方案。在HF休息时，心脏功能显着抑郁，并导致较低的平均动脉压，尽管增加HR。神经体液激活证明了肾脏和后肢血管收缩和NE，PRA和AVP水平升高，但它并没有增加在最温和的工作量。除轻度运动外，交感神经激活增加，伴有进行性肾血管收缩，RBF下降，NE、PRA和AVP大幅增加。随着运动强度的增加，外周血管收缩增加，导致动脉压升高到接近正常水平，尽管心输出量降低。然而，结合RBF的重定向，这并没有纠正后肢的灌注不足。我们的结论是，在HF狗，在休息时观察到的交感神经活动升高，并没有加剧轻度运动。然而，随着较重的工作负荷，交感神经激活开始于较低的工作负荷，并在较高的工作负荷逐渐扩大，从而改变血流的分布。
We hypothesized that performance of exercise during heart failure (HF) would lead to hypoperfusion of active skeletal muscles, causing sympathoactivation at lower workloads and alteration of the normal hemodynamic and hormonal responses. We measured cardiac output, mean aortic and right atrial pressures, hindlimb and renal blood flow (RBF), arterial plasma norepinephrine (NE), plasma renin activity (PRA), and plasma arginine vasopressin (AVP) in seven dogs during graded treadmill exercises and at rest. In control experiments, sympathetic activation at the higher workloads resulted in increased cardiac performance that matched the increased muscle vascular conductance. There were also increases in NE, PRA, and AVP. Renal vascular conductance decreased during exercise, such that RBF remained at resting levels. After control experiments, HF was induced by rapid ventricular pacing, and the exercise protocols were repeated. At rest in HF, cardiac performance was significantly depressed and caused lower mean arterial pressure, despite increased HR. Neurohumoral activation was evidenced by renal and hindlimb vasoconstriction and by elevated NE, PRA, and AVP levels, but it did not increase at the mildest workload. Beyond mild exercise, sympathoactivation increased, accompanied by progressive renal vasaconstriction, a fall in RBF, and very large increases of NE, PRA, and AVP. As exercise intensity increased, peripheral vasoconstriction increased, causing arterial pressure to rise to near normal levels, despite depressed cardiac output. However, combined with redirection of RBF, this did not correct the perfusion deficit to the hindlimbs. We conclude that, in dogs with HF, the elevated sympathetic activity observed at rest is not exacerbated by mild exercise. However, with heavier workloads, sympathoactivation begins at lower workloads and becomes progressively exaggerated at higher workloads, thus altering distribution of blood flow.