Potts J T, McKeown K P, Shoukas A A
Department of Physiology, Harry S. Moss Heart Center, University of Texas Southwestern Medical Center, Dallas 75235, USA.
Am J Physiol. 1998 Apr;274(4):H1121-31. doi: 10.1152/ajpheart.1998.274.4.H1121.
Baroreflex regulation of cardiac output is determined by the performance of the heart as well as the available blood flow returning to the heart (i.e., venous return). We hypothesized that a decrease in arterial compliance (C(a)) would affect carotid baroreflex control of cardiac output by altering the slope of the venous return curve (VR curve). Baroreflex control of systemic arterial pressure (Pa), central venous pressure (Pv), heart rate, cardiac output (CO), and peripheral vascular resistance (R) were determined during bilateral carotid occlusion (BCO) in spontaneously hypertensive (hypertensive, HT) and Sprague-Dawley (normotensive, NT) rats. C(a) was determined from the rate of arterial pressure decay when CO was transiently stopped, and the VR curve was obtained during graded inflation of a vascular balloon positioned in the right atrium. The inverse slope of the VR curve was used as an index of the resistance to venous return (RVR). The baseline slope of the VR curve was -50.5 +/- 3.3 vs. -35.5 +/- 2.6 ml.kg-1.min-1.mmHg-1 in NT vs. HT, respectively (P < 0.05). Control values of Pa (96 +/- 5 vs. 124 +/- 8 mmHg) and R [0.43 +/- 0.04 vs. 0.80 +/- 0.07 peripheral resistance units (PRU)] were reduced in NT, whereas Ca (0.062 +/- 0010 vs. 0.036 +/- 0.003 ml.kg-1.mmHg-1) was elevated in NT vs. HT, respectively (P < 0.05). Analysis of the pressure dependence of C(a) demonstrated that C(a) was a nonlinear function of Pa, and the exponential decay constant for the C(a)-Pa relationship was reduced in HT (0.0055 +/- 0.0012 vs. 0.0012 +/- 0.0002 min, NT vs. HT, P < 0.05). Baroreflex activation by BCO significantly increased Pa (delta Pa, 20 +/- 4 vs. 28 +/- 3 mmHg) and R (delta R, 0.16 +/- 0.04 vs. 0.24 +/- 0.06 PRU) in NT vs. HT, respectively. However, BCO significantly decreased CO in NT but not HT (delta CO, -24 +/- 5 vs. -4 +/- 6 ml.kg-1.min-1, P < 0.05). In NT, RVR was increased 39 +/- 9% during BCO (P < 0.05), whereas RVR increased 8 +/- 3% in HT (P = NS). From these findings, we conclude that the difference in baroreflex control of CO is mediated, in part, by the reduction in C(a), which minimized the baroreflex-evoked increase in RVR.
压力感受器反射对心输出量的调节取决于心脏的功能以及返回心脏的有效血流量（即静脉回心血量）。我们假设动脉顺应性（C(a)）降低会通过改变静脉回心血量曲线（VR曲线）的斜率来影响压力感受器反射对心输出量的控制。在双侧颈动脉闭塞（BCO）期间，测定了自发性高血压（高血压，HT）大鼠和斯普拉格-道利（正常血压，NT）大鼠的压力感受器反射对体动脉压（Pa）、中心静脉压（Pv）、心率、心输出量（CO）和外周血管阻力（R）的控制情况。C(a)通过在CO短暂停止时动脉压下降的速率来确定，VR曲线则在置于右心房的血管球囊分级充气期间获得。VR曲线的负斜率用作静脉回心血量阻力（RVR）的指标。NT组和HT组VR曲线的基线斜率分别为-50.5±3.3和-35.5±2.6 ml·kg⁻¹·min⁻¹·mmHg⁻¹（P<0.05）。NT组的Pa（96±5与124±8 mmHg）和R[0.43±0.04与0.80±0.07外周阻力单位（PRU）]的对照值降低，而NT组的C(a)（0.062±0.010与0.036±0.003 ml·kg⁻¹·mmHg⁻¹）高于HT组（P<0.05）。对C(a)的压力依赖性分析表明，C(a)是Pa的非线性函数，HT组中C(a)-Pa关系的指数衰减常数降低（NT组与HT组分别为0.0055±0.0012与0.0012±0.0002 min，P<0.05）。BCO激活压力感受器反射使NT组和HT组中的Pa（ΔPa，20±4与28±3 mmHg）和R（ΔR，0.16±0.04与0.24±0.06 PRU）分别显著升高。然而，BCO使NT组的CO显著降低，但HT组未降低（ΔCO，-24±5与-4±6 ml·kg⁻¹·min⁻¹，P<0.05）。在NT组中，BCO期间RVR增加39±9%（P<0.05），而HT组中RVR增加8±3%（P=无显著性差异）。根据这些发现，我们得出结论，压力感受器反射对CO控制的差异部分是由C(a)的降低介导的，这使压力感受器反射诱发的RVR增加最小化。
