Correlation between ventilation and brain blood flow during sleep.
Correlation between ventilation and brain blood flow during sleep.
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睡眠期间通气量与脑血流量之间的相关性。
DOI：
10.1172/jci111236
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发表时间：
1984
期刊：
影响因子：
--
通讯作者：
Edelman,NH
中科院分区：
文献类型：
--
作者：
Santiago,TV;Guerra,E;Neubauer,JA;Edelman,NH
对13只山羊睡眠时脑血流量(BBF)与通气量(VI)的关系进行了研究。用电磁流量探头连续测量单侧BBF，用放射性微球技术测定4只动物的整体和局部BBF。VI和BBF在慢波(SWS)和快速眼动(REM)睡眠中都发生了交互变化。在SWS期间，与清醒状态相比，VI显著降低，动脉血二氧化碳分压显著升高。SWS期间BBF与动脉二氧化碳分压(PaCO2)呈线性相关，且与清醒呼吸CO2的山羊相似。在REM睡眠期间，VI明显小于清醒(W)和SWS状态，这主要是由于潮气量的减少。与W和SWS状态相比，REM睡眠期间的BBF显著和显著增加；所有大脑区域都有这种增加。REM睡眠期间BBF的增加比PaCO2变化所预测的要大。在5只患有慢性矢状窦瘘的山羊中，在不同的研究中测量了动静脉氧差，发现在REM睡眠中，与W相比，REM睡眠中的脑氧耗显著降低；REM和W状态下的脑耗氧量相似。因此，快速眼动睡眠的高BBF也不能用大脑代谢活动的增加来解释。我们的结论是，在SWS期间，BBF的增加可以用低通气量和高碳酸血症来解释。相比之下，在REM睡眠期间，BBF远远超过PaCO2或大脑新陈代谢的预期。推测与SWS相比，REM睡眠中BBF的过多可能会降低中枢化学感受器的pH值。快速眼动睡眠期间对二氧化碳敏感性的降低和组织二氧化碳分压的降低相结合，使得在这种状态下中枢化学感受器的输出可能比SWS和清醒时要少。这可能是导致这一睡眠期潮气量低和呼吸不规律的原因。
The relationships between brain blood flow (BBF) and ventilation (VI) were studied during sleep in 13 goats. Unilateral BBF was continuously measured with an electromagnetic flow probe; total and regional BBF were assessed by the radioactive microsphere technique in four animals. Interacting changes in VI and BBF occurred during both slow wave (SWS) and rapid eye movement (REM) sleep. During SWS, significant decreases in VI and increases in arterial PCO2 occurred compared to wakefulness. BBF during SWS correlated linearly with arterial CO2 tension (PaCO2); nd the relationship was similar to that for awake goats breathing CO2. During REM sleep, VI was significantly less than both the awake (W) and SWS states due principally to a decrease in tidal volume. BBF during REM sleep was significantly and substantially increased compared with both the W and SWS states; this increase was shared by all brain areas. The increase in BBF during REM sleep was greater than that predicted from changes in PaCO2. In five goats provided with chronic sagittal sinus fistulae, arteriovenous oxygen difference was measured in separate studies and found to be significantly lower during REM sleep compared with W; brain O2 consumption was similar in magnitude in the REM and W states. Thus, the high BBF of REM sleep was also unexplained by an increase of brain metabolic activity. We conclude that, during SWS, increases in BBF are explained by hypoventilation and hypercapnia. In contrast, during REM sleep, BBF is substantially in excess of that expected from PaCO2 or brain metabolism. It is postulated that this excess of BBF during REM sleep could reduce the central chemoreceptor pH relative to that present in SWS. The combination of reduction of sensitivity to CO2 and lower tissue PCO2 during REM sleep makes it likely that the output of the central chemoreceptors during this state is less than that during SWS and wakefulness. This may contribute to the low tidal volume and respiratory irregularities of this sleep period.Images