Simmons Grant H, Manson Julie M, Halliwill John R
Department of Human Physiology, University of Oregon, Eugene, Oregon 97403-1240, USA.
J Physiol. 2007 Sep 15;583(Pt 3):1155-63. doi: 10.1113/jphysiol.2007.137216. Epub 2007 Jul 19.
We have previously shown that activation of peripheral chemoreceptors with isocapnic hypoxia resets arterial baroreflex control of heart rate and sympathetic vasoconstrictor outflow to higher pressures, without changes in baroreflex gain. We tested the hypothesis that activation of central chemoreceptors with mild hyperoxic hypercapnia also causes resetting of the arterial baroreflex, but that this resetting would not occur with matched volume and frequency hyperpnoea. Baroreflex control of heart rate (n = 16) and muscle sympathetic nerve activity (microneurography; n = 11) was assessed in healthy men and women, age 20-33 years, using the modified Oxford technique during hyperoxic eucapnia, hyperoxic hyperpnoea and hyperoxic hypercapnia (end-tidal P(CO(2)) + 5 mmHg above eucapnia). Baroreflex trials were separated by 30 min of rest. While neither hyperpnoea nor hypercapnia changed mean arterial pressure (92.0 +/- 1.8 during eucapnia versus 91.0 +/- 1.2 and 90.7 +/- 1.4 mmHg during hyperpnoea and hypercapnia; P = 0.427) or muscle sympathetic nerve activity (2,301 +/- 687 during eucapnia versus 2,959 +/- 987 and 2,272 +/- 414 total integrated units min(-1) during hyperpnoea and hypercapnia; P = 0.653), heart rate was increased from 59.3 +/- 2.7 during eucapnia to 63.2 +/- 3.0 and 62.4 +/- 2.8 beats min(-1) during hyperpnoea and hypercapnia (both P < 0.017). Baroreflex gain was not altered by hyperpnoea or hypercapnia. Thus, acute activation of central chemoreceptors with mild hyperoxic hypercapnia does not affect arterial pressure, sympathetic vasoconstrictor outflow, or baroreflex gain. Heart rate is elevated during hyperoxic hypercapnia, but this response is not different from the increase in heart rate produced by matched volume and frequency hyperpnoea. Therefore, mild activation of central chemoreceptors does not appear to alter arterial baroreflex function.
我们之前已经表明，等碳酸血症性低氧激活外周化学感受器会将动脉压力反射对心率和交感缩血管神经传出的控制重置为更高的压力水平，而压力反射增益不变。我们测试了以下假设：轻度高氧高碳酸血症激活中枢化学感受器也会导致动脉压力反射重置，但在匹配容量和频率的深呼吸时不会发生这种重置。在20 - 33岁的健康男性和女性中，采用改良牛津技术，在高氧正常碳酸血症、高氧深呼吸和高氧高碳酸血症（呼气末P(CO₂)比正常碳酸血症高5 mmHg）期间评估压力反射对心率（n = 16）和肌肉交感神经活动（微神经ography；n = 11）的控制。压力反射试验之间间隔30分钟休息时间。虽然深呼吸和高碳酸血症均未改变平均动脉压（正常碳酸血症时为92.0±1.8 mmHg，深呼吸和高碳酸血症时分别为91.0±1.2和90.7±1.4 mmHg；P = 0.427）或肌肉交感神经活动（正常碳酸血症时为2,301±687总积分单位·分钟⁻¹，深呼吸和高碳酸血症时分别为2,959±987和2,272±414总积分单位·分钟⁻¹；P = 0.653），但心率从正常碳酸血症时的59.3±2.7次/分钟增加到深呼吸和高碳酸血症时的63.2±3.0和62.4±2.8次/分钟（两者P均<0.017）。压力反射增益未因深呼吸或高碳酸血症而改变。因此，轻度高氧高碳酸血症急性激活中枢化学感受器不会影响动脉血压、交感缩血管神经传出或压力反射增益。高氧高碳酸血症期间心率升高，但这种反应与匹配容量和频率的深呼吸所产生的心率增加无差异。因此，中枢化学感受器的轻度激活似乎不会改变动脉压力反射功能。
