Mannozzi Joseph, Al-Hassan Mohamed-Hussein, Kaur Jasdeep, Lessanework Beruk, Alvarez Alberto, Massoud Louis, Bhatti Tauheed, O'Leary Donal S
Department of Physiology, Wayne State University School of Medicine, Detroit, MI, United States.
Department of Kinesiology and Health Education, University of Texas at Austin, Austin, TX, United States.
Front Physiol. 2022 Apr 5;13:835951. doi: 10.3389/fphys.2022.835951. eCollection 2022.
Autonomic alterations in blood pressure are primarily a result of arterial baroreflex modulation of systemic vascular resistance and cardiac output on a beat-by-beat basis. The combined central and peripheral control by the baroreflex likely acts to maintain efficient energy transfer from the heart to the systemic vasculature; termed ventricular-vascular coupling. This level of control is maintained whether at rest or during exercise in healthy subjects. During heart failure, the ventricular-vascular relationship is uncoupled and baroreflex dysfunction is apparent. We investigated if baroreflex dysfunction in heart failure exacerbated ventricular-vascular uncoupling at rest, and during exercise in response to baroreceptor unloading by performing bilateral carotid occlusions in chronically instrumented conscious canines. We observed in healthy subjects that baroreceptor unloading caused significant increases in effective arterial elastance (Ea) at rest (1.2 ± 0.3 mmHg/ml) and during exercise (1.3 ± 0.2 mmHg/ml) that coincided with significant increases in stroke work (SW) (1.5 ± 0.2 mmHg/ml) and (1.6 ± 0.2 mmHg/ml) suggesting maintained ventricular-vascular coupling. Heart Failure significantly increased the effect of baroreceptor unloading on Ea at rest (3.1 ± 0.7 mmHg/ml) and during exercise (2.3 ± 0.5 mmHg/ml) whereas no significant increases in stroke work occurred, thus signifying further ventricular-vascular uncoupling. We believe that the enhanced ventricular-vascular uncoupling observed during baroreceptor unloading only worsens the already challenged orthostatic and exercise tolerance and thereby contributes to poor exercise performance and quality of life for heart failure patients.
血压的自主神经改变主要是由于动脉压力反射在逐搏基础上对全身血管阻力和心输出量进行调节的结果。压力反射的中枢和外周联合控制可能起到维持从心脏到全身血管系统有效能量传递的作用；这被称为心室-血管耦合。在健康受试者中，无论处于静息状态还是运动期间，这种控制水平都会维持。在心力衰竭期间，心室-血管关系解耦，压力反射功能障碍明显。我们通过对长期植入仪器的清醒犬进行双侧颈动脉闭塞，研究心力衰竭时的压力反射功能障碍是否会在静息时以及运动期间因压力感受器卸载而加剧心室-血管解耦。我们观察到，在健康受试者中，压力感受器卸载会导致静息时（1.2±0.3 mmHg/ml）和运动期间（1.3±0.2 mmHg/ml）有效动脉弹性（Ea）显著增加，这与每搏功（SW）显著增加（1.5±0.2 mmHg/ml）和（1.6±0.2 mmHg/ml）同时出现，表明心室-血管耦合得以维持。心力衰竭显著增加了压力感受器卸载对静息时（3.1±0.7 mmHg/ml）和运动期间（2.3±0.5 mmHg/ml）Ea的影响，而每搏功没有显著增加，从而表明心室-血管进一步解耦。我们认为，在压力感受器卸载期间观察到的增强的心室-血管解耦只会使已经受到挑战的直立耐受性和运动耐受性恶化，从而导致心力衰竭患者运动能力差和生活质量低。
