Changes in human cerebral blood flow and cerebral blood volume during hypercapnia and hypocapnia measured by positron emission tomography
Changes in human cerebral blood flow and cerebral blood volume during hypercapnia and hypocapnia measured by positron emission tomography
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DOI：
10.1097/01.wcb.0000067721.64998.f5
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发表时间：
2003-06-01
影响因子：
6.3
通讯作者：
Miura, S
中科院分区：
文献类型：
--
作者：
Ito, H;Kanno, I;Miura, S
高碳酸血症诱导脑血管舒张并增加脑血流量（CBF），低碳酸血症诱导脑血管收缩并降低CBF。然而，在人类高碳酸血症和低碳酸血症期间CBF和脑血容量（CBV）变化之间的关系尚不清楚。在9名健康受试者中，通过正电子发射断层扫描测量了静息时和高碳酸血症和低碳酸血症期间的CBF和CBV。根据CBF和CBV，对高碳酸血症的血管反应分别为6.0 +/- 2.6%/mm Hg和1.8 +/- 1.3%/mm Hg，对低碳酸血症的血管反应分别为-3.5 +/- 0.6%/mm Hg和-1.3 +/- 1.0%/mm Hg。CBF与CBV之间的关系为CBV = 1.09 CBF 0.29。在高碳酸血症期间，CBF的增加大于CBV的增加，表明血管血流速度增加。低碳酸血症时CBF下降的程度大于CBV，表明血管血流速度降低。高碳酸血症期间CBF和CBV的变化之间的关系是类似的，在神经激活，但是，在低碳酸血症期间的关系是不同的，在神经失活期间观察到的交叉小脑神经不能。这表明CBF和CBV的增加可能受神经激活和高碳酸血症之间类似的微循环机制的控制，但CBF和CBV的减少可能受神经失活和低碳酸血症之间不同的机制的控制。
Hypercapnia induces cerebral vasodilation and increases cerebral blood flow (CBF), and hypocapnia induces cerebral vasoconstriction and decreases CBF. The relation between changes in CBF and cerebral blood volume(CBV) during hypercapnia and hypocapnia in humans, however, is not clear. Both CBF and CBV were measured at rest and during hypercapnia and hypocapnia in nine healthy subjects by positron emission tomography. The vascular responses to hypercapnia in terms of CBF and CBV were 6.0 +/- 2.6%/mm Hg and 1.8 +/- 1.3%/mm Hg, respectively, and those to hypocapnia were -3.5 +/- 0.6%/mm Hg and -1.3 +/- 1.0%/mm Hg, respectively. The relation between CBF and CBV was CBV = 1.09 CBF0.29. The increase in CBF was greater than that in CBV during hypercapnia, indicating an increase in vascular blood velocity. The degree of decrease in CBF during hypocapnia was greater than that in CBV, indicating a decrease in vascular blood velocity. The relation between changes in CBF and CBV during hypercapnia was similar to that during neural activation; however, the relation during hypocapnia was different from that during neural deactivation observed in crossed cerebellar diaschisis. This suggests that augmentation of CBF and CBV might be governed by a similar microcirculatory mechanism between neural activation and hypercapnia, but diminution of CBF and CBV might be governed by a different mechanism between neural deactivation and hypocapnia.