Sala-Mercado Javier A, Moslehpour Mohsen, Hammond Robert L, Ichinose Masashi, Chen Xiaoxiao, Evan Sell, O'Leary Donal S, Mukkamala Ramakrishna
Department of Physiology and Cardiovascular Research Institute, Wayne State University School of Medicine, Detroit, Michigan; and.
Department of Electrical and Computer Engineering, Michigan State University, East Lansing, Michigan.
Am J Physiol Regul Integr Comp Physiol. 2014 Aug 15;307(4):R455-64. doi: 10.1152/ajpregu.00510.2013. Epub 2014 Jun 18.
The cardiopulmonary baroreflex responds to an increase in central venous pressure (CVP) by decreasing total peripheral resistance and increasing heart rate (HR) in dogs. However, the direction of ventricular contractility change is not well understood. The aim was to elucidate the cardiopulmonary baroreflex control of ventricular contractility during normal physiological conditions via a mathematical analysis. Spontaneous beat-to-beat fluctuations in maximal ventricular elastance (Emax), which is perhaps the best available index of ventricular contractility, CVP, arterial blood pressure (ABP), and HR were measured from awake dogs at rest before and after β-adrenergic receptor blockade. An autoregressive exogenous input model was employed to jointly identify the three causal transfer functions relating beat-to-beat fluctuations in CVP to Emax (CVP → Emax), which characterizes the cardiopulmonary baroreflex control of ventricular contractility, ABP to Emax, which characterizes the arterial baroreflex control of ventricular contractility, and HR to Emax, which characterizes the force-frequency relation. The CVP → Emax transfer function showed a static gain of 0.037 ± 0.010 ml(-1) (different from zero; P < 0.05) and an overall time constant of 3.2 ± 1.2 s. Hence, Emax would increase and reach steady state in ∼16 s in response to a step increase in CVP, without any change to ABP or HR, due to the cardiopulmonary baroreflex. Following β-adrenergic receptor blockade, the CVP → Emax transfer function showed a static gain of 0.0007 ± 0.0113 ml(-1) (different from control; P < 0.10). Hence, Emax would change little in steady state in response to a step increase in CVP. Stimulation of the cardiopulmonary baroreflex increases ventricular contractility through β-adrenergic receptor system mediation.
在犬类中，心肺压力反射通过降低总外周阻力和增加心率（HR）来应对中心静脉压（CVP）的升高。然而，心室收缩性变化的方向尚未完全明确。本研究旨在通过数学分析阐明正常生理条件下心肺压力反射对心室收缩性的控制。在β-肾上腺素能受体阻断前后，测量清醒静息犬的最大心室弹性（Emax，这可能是衡量心室收缩性的最佳指标）、CVP、动脉血压（ABP）和HR的逐搏自发波动。采用自回归外生输入模型共同识别三个因果传递函数，分别为CVP逐搏波动与Emax之间的函数（CVP→Emax），其表征心肺压力反射对心室收缩性的控制；ABP与Emax之间的函数，其表征动脉压力反射对心室收缩性的控制；以及HR与Emax之间的函数，其表征力-频率关系。CVP→Emax传递函数的静态增益为0.037±0.010 ml⁻¹（与零不同；P<0.05），总时间常数为3.2±1.2 s。因此，由于心肺压力反射，CVP的阶跃增加会使Emax在约16 s内增加并达到稳态，而ABP或HR无任何变化。β-肾上腺素能受体阻断后，CVP→Emax传递函数的静态增益为0.0007±0.0113 ml⁻¹（与对照组不同；P<0.10）。因此，CVP的阶跃增加时，Emax在稳态下变化很小。心肺压力反射的刺激通过β-肾上腺素能受体系统介导增加心室收缩性。
