Department of Neuroscience, University of Minnesota, Minneapolis, MN 55455, USA.
Proc Natl Acad Sci U S A. 2011 Oct 25;108(43):17827-31. doi: 10.1073/pnas.1110533108. Epub 2011 Oct 17.
Neurovascular coupling is a process through which neuronal activity leads to local increases in blood flow in the central nervous system. In brain slices, 100% O(2) has been shown to alter neurovascular coupling, suppressing activity-dependent vasodilation. However, in vivo, hyperoxia reportedly has no effect on blood flow. Resolving these conflicting findings is important, given that hyperoxia is often used in the clinic in the treatment of both adults and neonates, and a reduction in neurovascular coupling could deprive active neurons of adequate nutrients. Here we address this issue by examining neurovascular coupling in both ex vivo and in vivo rat retina preparations. In the ex vivo retina, 100% O(2) reduced light-evoked arteriole vasodilations by 3.9-fold and increased vasoconstrictions by 2.6-fold. In vivo, however, hyperoxia had no effect on light-evoked arteriole dilations or blood velocity. Oxygen electrode measurements showed that 100% O(2) raised pO(2) in the ex vivo retina from 34 to 548 mm Hg, whereas hyperoxia has been reported to increase retinal pO(2) in vivo to only ~53 mm Hg [Yu DY, Cringle SJ, Alder VA, Su EN (1994) Am J Physiol 267:H2498-H2507]. Replicating the hyperoxic in vivo pO(2) of 53 mm Hg in the ex vivo retina did not alter vasomotor responses, indicating that although O(2) can modulate neurovascular coupling when raised sufficiently high, the hyperoxia-induced rise in retinal pO(2) in vivo is not sufficient to produce a modulatory effect. Our findings demonstrate that hyperoxia does not alter neurovascular coupling in vivo, ensuring that active neurons receive an adequate supply of nutrients.
神经血管耦联是一个过程，其中神经元活动导致中枢神经系统中的局部血流增加。在脑切片中，已经表明 100%的 O(2)会改变神经血管耦联，抑制与活动相关的血管扩张。然而，在体内，高氧据称对血流没有影响。解决这些相互矛盾的发现很重要，因为高氧在临床上经常用于治疗成人和新生儿，并且神经血管耦联的减少可能会使活跃的神经元缺乏足够的营养。在这里，我们通过检查离体和体内大鼠视网膜准备物中的神经血管耦联来解决这个问题。在离体视网膜中，100%的 O(2)将光诱发的小动脉血管扩张减少了 3.9 倍，并增加了 2.6 倍的血管收缩。然而，在体内，高氧对光诱发的小动脉扩张或血流速度没有影响。氧电极测量表明，100%的 O(2)将离体视网膜中的 pO(2)从 34 升高到 548 毫米汞柱，而高氧已被报道在体内仅将视网膜 pO(2)升高到约 53 毫米汞柱[Yu DY，Cringle SJ，Alder VA，Su EN（1994）Am J Physiol 267：H2498-H2507]。在离体视网膜中复制 53 毫米汞柱的高氧体内 pO(2)不会改变血管运动反应，表明尽管当氧升高到足够高时可以调节神经血管耦联，但体内视网膜 pO(2)的高氧诱导升高不足以产生调节作用。我们的发现表明，高氧不会改变体内的神经血管耦联，从而确保活跃的神经元获得足够的营养供应。
