Bao G, Randhawa P M, Fletcher E C
Department of Medicine, Louisville Veterans Affairs Medical Center and University of Louisville School of Medicine, Kentucky 40292, USA.
J Appl Physiol (1985). 1997 Apr;82(4):1071-8. doi: 10.1152/jappl.1997.82.4.1071.
Using a rat model, we investigated whether episodic eucapnic hypoxia was a more potent stimulus to acute blood pressure (BP) elevation and bradycardia than episodic hypocapnic hypoxia. We also investigated the role of sympathetic and parasympathetic nervous system in this cardiovascular response. Sprague-Dawley (SD) and Wistar Kyoto (WKY) rats were exposed to repetitive 30-s cycles of hypocapnic or eucapnic hypoxia before and after intravenous injection of the alpha1-adrenergic blocker prazosin, alpha2-adrenergic blocker yohimbine, or atropine. Eucapnic hypoxia caused a threefold elevation in systolic BP from baseline (83.5 +/- 3.5 mmHg in WKY, 70.6 +/- 4.6 mmHg in SD) and greater bradycardia (-178 +/- 20 beats/min in WKY, -178 +/- 21 beats/min in SD) compared with hypocapnic hypoxia (29.8 +/- 3.6 mmHg and -43 +/- 15 beats/min in WKY, 19.0 +/- 4.1 mmHg and -45 +/- 12 beats/min in SD). After prazosin, the BP increase from eucapnic hypoxia was blunted, yohimbine showed no effect, and atropine blocked the bradycardia. Direct measurement of sympathetic nerve activity confirmed that adding CO2 to the hypoxic gas mixture caused a 61% increase in sympathetic nerve activity. WKY rats seem more vulnerable than SD rats to both hypoxia exposures in terms of the elevation in BP. We conclude that, in the rat, eucapnic hypoxia is a more potent stimulus to acute BP elevation and bradycardia than is hypocapnic hypoxia. An increased sympathetic tone appears to be involved in the BP response to acute episodic hypoxia.
利用大鼠模型，我们研究了间歇性等碳酸血症性低氧相较于间歇性低碳酸血症性低氧是否是急性血压（BP）升高和心动过缓的更强有力刺激因素。我们还研究了交感神经系统和副交感神经系统在这种心血管反应中的作用。在静脉注射α1肾上腺素能阻滞剂哌唑嗪、α2肾上腺素能阻滞剂育亨宾或阿托品之前及之后，将斯普拉格-道利（SD）大鼠和威斯塔·京都（WKY）大鼠暴露于重复性30秒的低碳酸血症或等碳酸血症性低氧周期中。与低碳酸血症性低氧相比（WKY大鼠中为29.8±3.6 mmHg和-43±15次/分钟，SD大鼠中为19.0±4.1 mmHg和-45±12次/分钟），等碳酸血症性低氧使收缩压较基线升高了三倍（WKY大鼠中从基线的83.5±3.5 mmHg升高，SD大鼠中从基线的70.6±4.6 mmHg升高），且心动过缓更明显（WKY大鼠中为-178±20次/分钟，SD大鼠中为-178±21次/分钟）。注射哌唑嗪后，等碳酸血症性低氧引起的血压升高减弱，育亨宾无作用，阿托品则阻断了心动过缓。交感神经活动的直接测量证实，向低氧气体混合物中添加二氧化碳使交感神经活动增加了61%。就血压升高而言，WKY大鼠似乎比SD大鼠对两种低氧暴露都更敏感。我们得出结论，在大鼠中，等碳酸血症性低氧相较于低碳酸血症性低氧是急性血压升高和心动过缓的更强有力刺激因素。交感神经张力增加似乎参与了对急性间歇性低氧的血压反应。
