Lai C J, Yang C C H, Hsu Y Y, Lin Y N, Kuo T B J
Institute of Neuroscience, Department of Physiology, Tzu-Chi University, Hualien, Taiwan.
J Appl Physiol (1985). 2006 Jun;100(6):1974-82. doi: 10.1152/japplphysiol.01051.2005. Epub 2006 Feb 16.
Long-term exposure to intermittent hypoxia (IH), such as that occurring in association with sleep apnea, may result in systemic hypertension; however, the time course changes in arterial pressure, autonomic functions, and baroreflex sensitivity are still unclear. We investigated the changes in cardiovascular neural regulations during the development of chronic IH-induced hypertension in rats. Sprague-Dawley rats were exposed to repetitive 1.25-min cycles (30 s of N2+45 s of 21% O2) of IH or room air (RA) for 6 h/day during light phase (10 AM-4 PM) for 30 days. Arterial pressure was measured daily using the telemetry system during RA breathing. The mean arterial pressure (MAP) and interpulse interval (PPI) signals were then used to assess the autonomic functions and spontaneous baroreflex sensitivity by auto- and cross-spectral analysis, respectively. Stable MAP, low-frequency power of MAP (BLF), and low-frequency power (LF)-to-high frequency power (HF) ratio of PPI (LF/HF) were significantly higher in IH-exposed rats, compared with those of RA-exposed rats. Elevation of the MAP, BLF, LF/HF, and minute ventilation started 5 days after IH exposure and lasted until the end of the 30-day observation period. Additionally, IH-exposed rats had significant lower slope of MAP-PPI linear regression (under a successively descending and ascending) and magnitude of MAP-PPI transfer function (at frequency ranges of 0.06-0.6 Hz or 0.6-2.4 Hz) after IH exposure for 17 days. However, RA-exposed rats did not exhibit these changes. The results of this study indicate that chronic IH-induced hypertension is associated with a facilitation of cardiovascular sympathetic outflow and inhibition of baroreflex sensitivity in conscious rats.
长期暴露于间歇性低氧（IH），如与睡眠呼吸暂停相关的情况，可能会导致全身性高血压；然而，动脉血压、自主神经功能和压力反射敏感性的时间进程变化仍不清楚。我们研究了大鼠慢性IH诱导的高血压发展过程中心血管神经调节的变化。将Sprague-Dawley大鼠在光照期（上午10点至下午4点）每天暴露于重复的1.25分钟周期（30秒氮气+45秒21%氧气）的IH或室内空气（RA）中，持续6小时，共30天。在RA呼吸期间，每天使用遥测系统测量动脉血压。然后分别通过自谱和互谱分析，使用平均动脉压（MAP）和脉冲间期（PPI）信号来评估自主神经功能和自发压力反射敏感性。与暴露于RA的大鼠相比，暴露于IH的大鼠的稳定MAP、MAP的低频功率（BLF）以及PPI的低频功率（LF）与高频功率（HF）之比（LF/HF）显著更高。MAP、BLF、LF/HF和分钟通气量在暴露于IH后5天开始升高，并持续到30天观察期结束。此外，暴露于IH 17天后，暴露于IH的大鼠的MAP-PPI线性回归斜率（在连续下降和上升时）和MAP-PPI传递函数幅度（在0.06-0.6 Hz或0.6-2.4 Hz频率范围内）显著降低。然而，暴露于RA的大鼠未出现这些变化。本研究结果表明，慢性IH诱导的高血压与清醒大鼠心血管交感神经输出的促进和压力反射敏感性的抑制有关。
