Independent cerebral vasoconstrictive effects of hyperoxia and accompanying arterial hypocapnia at 1 ATA
Independent cerebral vasoconstrictive effects of hyperoxia and accompanying arterial hypocapnia at 1 ATA
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DOI：
10.1152/japplphysiol.00303.2003
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发表时间：
2003-12-01
影响因子：
3.3
通讯作者：
Eckenhoff, RG
中科院分区：
文献类型：
--
作者：
Floyd, TF;Clark, JM;Eckenhoff, RG
已知在1个大气压绝对压力（ATA）下呼吸100% O-2与脑血流量（CBF）减少有关。它还伴随着动脉PCO 2的下降，导致不确定脑血管收缩是否完全或仅部分由动脉低碳酸血症引起。我们检验了以下假设：在1.0 ATA下呼吸O-2时，动脉PO 2的增加会降低CBF，而与动脉PCO 2的同时下降无关。使用无创连续动脉自旋标记灌注MRI测量7名年龄在21-62岁的健康男性的CBF。该技术中的示踪剂，血液中的磁性标记质子，具有秒的半衰期，允许在短时间内重复测量而不受污染。在呼吸空气、100%O-2以及空气和O-2背景中的4%和6%CO2时测量CBF和动脉血气。动脉PO 2从空气中的91.7 +/- 6.8 Torr增加到O-2中的576.7 +/- 18.9 Torr。动脉PCO 2从空气中的43.3 +/- 1.8 Torr下降到O-2中的40.2 +/- 3.3 Torr，空气和高氧运行的CBF-动脉PCO 2响应曲线几乎平行，并相隔一段距离，代表CBF减少28.7-32.6%。回归分析证实了动脉PO 2增加的独立脑血管收缩效应。目前的结果还表明，在1.0 ATA的这种影响的幅度大于先前测量的。
Breathing 100% O-2 at 1 atmosphere absolute (ATA) is known to be associated with a decrease in cerebral blood flow (CBF). It is also accompanied by a fall in arterial PCO2 leading to uncertainty as to whether the cerebral vasoconstriction is totally or only in part caused by arterial hypocapnia. We tested the hypothesis that the increase in arterial PO2 while O-2 was breathed at 1.0 ATA decreases CBF independently of a concurrent fall in arterial PCO2. CBF was measured in seven healthy men aged 21-62 yr by using noninvasive continuous arterial spin-labeled-perfusion MRI. The tracer in this technique, magnetically labeled protons in blood, has a half-life of seconds, allowing repetitive measurements over short time frames without contamination. CBF and arterial blood gases were measured while breathing air, 100% O-2, and 4 and 6% CO2 in air and O-2 backgrounds. Arterial PO2 increased from 91.7 +/- 6.8 Torr in air to 576.7 +/- 18.9 Torr in O-2. Arterial PCO2 fell from 43.3 +/- 1.8 Torr in air to 40.2 +/- 3.3 Torr in O-2, CBF-arterial PCO2 response curves for the air and hyperoxic runs were nearly parallel and separated by a distance representing a 28.7-32.6% decrement in CBF. Regression analysis confirmed the independent cerebral vasoconstrictive effect of increased arterial PO2. The present results also demonstrate that the magnitude of this effect at 1.0 ATA is greater than previously measured.