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Beat-to-beat autonomic cardiovascular response to short-term 10002 breathing: A time-frequency analysis approach

机译:击败自动心血管反应短期100%02呼吸:时频分析方法

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In sixteen healthy volunteers, we assessed the effects produced by short-term 100% O2 breathing on the instantaneous time courses of R-R intervals (RR), arterial pressure (AP), arterial oxygen saturation (SaO2), respiratory volume (Res), and, estimated by a time frequency distribution, the high frequency powers of RR (HFrr) and Res (HFRes), the low frequency powers of RR (LFrr) and systolic pressure (LFSP), the LFRR/HFRR ratio, baroreflex sensitivity (BRS) by alpha index and respiratory sinus arrhythmia sensitivity (RSAS). Short-time hyperoxemia provoked various effects with different latencies: a) RR lengthening, with 15-s latency; b) AP increase, with 75-s latency, c) BRS and RSAS increases with 120-s latency, d) HFrr increase and LFSP and LFrr/HFrr decreases, with 135-s latency, and d) no significant changes on Res. During hyperoxemia, the instantaneous time courses of these variables are fluctuating, with subtle yet significant changes at different latencies. Initially, hyperoxemia lengthens RR by direct inhibition of the sinoatrial node, and later on, it elicits a direct vasoconstriction-dependent increment of AP, which, via baroreflex with augmented sensitivity, increases vagal outflow and reduces sympathetic activity, changes strengthened by the augmented RSAS, but hyperoxemia does not modify the respiratory variables.
机译:在十六份健康的志愿者中,我们评估了在RR间隔(RR),动脉压(AP),动脉氧饱和度(SAO2),呼吸体积(RES)和呼吸体积(RES)的瞬时时间课程中通过短期100%O2呼吸产生的效果。 ,通过时间频率分布,RR(HFRR)和RE(HFRE)的高频功率,RR(LFRR)的低频功率(LFRR)和收缩压(LFSP),LFRR / HFRR比,Baroreflex敏感度(BRS)通过α指数和呼吸窦性心律失常(RSAS)。短时性高氧血症引发了不同延迟的各种效果:a)RR延长,延迟15秒; b)随着75-S等待时间的增加,C)BRS和RSA随120-S等待时间而增加,D)HFRR增加和LFSP和LFRR / HFRR降低,具有135秒的延迟和d)RES对RE没有显着变化。在高血管血症期间,这些变量的瞬时时间课程是波动的,不同延迟的微妙但显着变化。最初,通过直接抑制SINOOTIAL节点和后来的高血症延长RR,它引起了AP的直接血管收缩依赖性增量,这通过苦参克隆具有增强敏感性,增加了迷走流出并减少了增强RSA的改变加强的变化,但高血清症不会改变呼吸变量。

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