Kurtz Theodore W, Lujan Heidi L, DiCarlo Stephen E
Department of Laboratory Medicine, University of California, San Francisco, San Francisco, California.
Department of Physiology, Wayne State University School of Medicine, Detroit, Michigan.
Physiol Rep. 2014 Nov 26;2(11). doi: 10.14814/phy2.12223. Print 2014 Nov 1.
Few studies have systematically investigated whether daily patterns of arterial blood pressure over 24 h are mediated by changes in cardiac output, peripheral resistance, or both. Understanding the hemodynamic mechanisms that determine the 24 h patterns of blood pressure may lead to a better understanding of how such patterns become disturbed in hypertension and influence risk for cardiovascular events. In conscious, unrestrained C57BL/6J mice, we investigated whether the 24 h pattern of arterial blood pressure is determined by variation in cardiac output, systemic vascular resistance, or both and also whether variations in cardiac output are mediated by variations in heart rate and or stroke volume. As expected, arterial pressure and locomotor activity were significantly (P < 0.05) higher during the nighttime period compared with the daytime period when mice are typically sleeping (+12.5 ± 1.0 mmHg, [13%] and +7.7 ± 1.3 activity counts, [254%], respectively). The higher arterial pressure during the nighttime period was mediated by higher cardiac output (+2.6 ± 0.3 mL/min, [26%], P < 0.05) in association with lower peripheral resistance (-1.5 ± 0.3 mmHg/mL/min, [-13%] P < 0.05). The increased cardiac output during the nighttime was mainly mediated by increased heart rate (+80.0 ± 16.5 beats/min, [18%] P < 0.05), as stroke volume increased minimally at night (+1.6 ± 0.5 μL per beat, [6%] P < 0.05). These results indicate that in C57BL/6J mice, the 24 h pattern of blood pressure is hemodynamically mediated primarily by the 24 h pattern of cardiac output which is almost entirely determined by the 24 h pattern of heart rate. These findings suggest that the differences in blood pressure between nighttime and daytime are mainly driven by differences in heart rate which are strongly correlated with differences in locomotor activity.
很少有研究系统地调查过24小时动脉血压的日常模式是否由心输出量、外周阻力或两者的变化所介导。了解决定24小时血压模式的血流动力学机制，可能有助于更好地理解这些模式在高血压中是如何受到干扰的，以及如何影响心血管事件的风险。在清醒、不受约束的C57BL/6J小鼠中，我们研究了24小时动脉血压模式是由心输出量、全身血管阻力或两者的变化所决定的，以及心输出量的变化是否由心率和/或每搏输出量的变化所介导。正如预期的那样，与白天小鼠通常睡觉的时间段相比，夜间的动脉压和运动活动显著更高（P<0.05）（分别为+12.5±1.0 mmHg，[13%]和+7.7±1.3活动计数，[254%]）。夜间较高的动脉压是由较高的心输出量（+2.6±0.3 mL/分钟，[26%]，P<0.05）和较低的外周阻力（-1.5±0.3 mmHg/mL/分钟，[-13%]，P<0.05）介导的。夜间心输出量的增加主要由心率增加（+80.0±16.5次/分钟，[18%]，P<0.05）介导，因为夜间每搏输出量增加最小（+1.6±0.5 μL/次搏动，[6%]，P<0.05）。这些结果表明，在C57BL/6J小鼠中，24小时血压模式主要由心输出量的24小时模式血流动力学介导，而心输出量的24小时模式几乎完全由心率的24小时模式决定。这些发现表明，夜间和白天血压的差异主要由心率差异驱动，而心率差异与运动活动差异密切相关。
