Marcus Noah J, Olson E Burt, Bird Cynthia E, Philippi Nathan R, Morgan Barbara J
John Rankin Laboratory of Pulmonary Medicine, Department of Kinesiology, Respiratory Neurobiology Training Program, University of Wisconsin, Madison, WI, USA.
Respir Physiol Neurobiol. 2009 Jan 1;165(1):90-6. doi: 10.1016/j.resp.2008.10.013. Epub 2008 Nov 1.
In rats, acute exposure to hypoxia causes a decrease in mean arterial pressure (MAP) caused by a predominance of hypoxic vasodilation over chemoreflex-induced vasoconstriction. We previously demonstrated that exposure to chronic intermittent hypoxia (CIH) impairs hypoxic vasodilation in isolated resistance arteries; therefore, we hypothesized that the acute systemic hemodynamic responses to hypoxia would be altered by exposure to CIH. To test this hypothesis, rats were exposed to CIH for 14 days. Heart rate (HR) and MAP were monitored by telemetry. On the first day of CIH exposure, acute episodes of hypoxia caused a decrease in MAP (-9+/-5 mmHg) and an increase in HR (+45+/-4 beats/min). On the 14th day of CIH exposure the depressor response was attenuated (-4+/-1mmHg; 44% of the day 1 response) and the tachycardia was enhanced (+68+/-2 beats/min; 151% of the day 1 response). The observed time-dependent modulation of the acute hemodynamic responses to hypoxia may reflect important changes in neurocirculatory regulation that contribute to CIH-induced hypertension.
在大鼠中,急性缺氧会导致平均动脉压(MAP)下降,这是由于缺氧性血管舒张占主导地位,超过了化学反射诱导的血管收缩。我们之前证明,暴露于慢性间歇性缺氧(CIH)会损害离体阻力动脉的缺氧性血管舒张;因此,我们假设暴露于CIH会改变对缺氧的急性全身血流动力学反应。为了验证这一假设,将大鼠暴露于CIH 14天。通过遥测监测心率(HR)和MAP。在暴露于CIH的第一天,急性缺氧发作导致MAP下降(-9±5 mmHg)和HR增加(+45±4次/分钟)。在暴露于CIH的第14天,降压反应减弱(-4±1 mmHg;第1天反应的44%),心动过速增强(+68±2次/分钟;第1天反应的151%)。观察到的对缺氧的急性血流动力学反应的时间依赖性调节可能反映了神经循环调节的重要变化,这些变化导致了CIH诱导的高血压。