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首页> 外文期刊>Hypertension research: Official journal of the Japanese Society of Hypertension >Deactivation of carotid body chemoreceptors by hyperoxia decreases blood pressure in hypertensive patients
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Deactivation of carotid body chemoreceptors by hyperoxia decreases blood pressure in hypertensive patients

机译:高氧使颈动脉体化学感受器失活可降低高血压患者的血压

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Previous studies have shown that hyperoxia-induced deactivation of carotid body chemoreceptors reduces sympathetic activity in hypertensive patients but it does not affect blood pressure. The maintenance of blood pressure can be explained by the direct, vasoconstrictive effect of hyperoxia, which offsets diminished sympathetic activity. This study compares the effect of acute hyperoxia on hemodynamic parameters between hypertensive and normotensive subjects. Twelve males with hypertension (age 39.4 +-2.4 years; body mass index 27.4 +- 1.1 kg m~(-2)) and 11 normotensive males (age 39.9 +-2.7 years; body mass index 25.4 +-0.7 kg m~(-2)) received, via non-rebreathing mask ventilation, ambient air, followed by 100% oxygen for 20 min. The stroke volume, heart rate, cardiac output, blood pressure, total peripheral resistance, respiratory rate, baroreceptor control of heart rate and oxygen saturation were recorded continuously. Several 30 s periods were analyzed before, during and after inducing hyperoxia. At baseline, the hypertensive subject's blood pressure was higher and their baroreflex control of heart rate was lower when compared with the normotensive control group. After the first 30s of hyperoxia, systolic, diastolic and mean blood pressures, as well as the total peripheral resistance, decreased significantly in hypertensives but not in normotensives. After 20 min of 100% oxygen ventilation, systolic and mean blood pressures and total peripheral resistance was increased in hypertensive patients, and the cardiac output and stroke volume had decreased in both groups. The results of this study confirm that deactivation of carotid body chemoreceptors can acutely decrease blood pressure in humans.
机译:先前的研究表明,高氧诱导的颈动脉体化学感受器失活可降低高血压患者的交感神经活动,但不会影响血压。血压的维持可以由高氧的直接血管收缩作用解释,该作用可以抵消交感神经活动的减弱。这项研究比较了急性高氧对高血压和正常血压受试者血液动力学参数的影响。十二名患有高血压的男性(年龄39.4±2.4岁;体重指数27.4±1.1 kg m〜(-2))和11名血压正常的男性(年龄39.9±-2.7岁;体重指数25.4±0.7kg·m〜(-2) -2))通过无呼吸面罩通气接收环境空气,然后用100%氧气保持20分钟。连续记录中风量,心率,心输出量,血压,总外周阻力,呼吸频率,心率的压力感受器控制和氧饱和度。在诱发高氧之前,期间和之后分析了30 s的时间。与正常血压对照组相比,在基线时,高血压受试者的血压较高,对心律的压力反射控制较低。在高氧的最初30秒钟后,高血压患者的收缩压,舒张压和平均血压以及总的外周阻力显着降低,而正常血压则没有降低。在100%氧气通气20分钟后,高血压患者的收缩压和平均血压以及总外周阻力增加,两组的心输出量和中风量均降低。这项研究的结果证实,颈动脉体化学感受器的失活可以急剧降低人的血压。

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