Capillary pericytes regulate cerebral blood flow in health and disease.
Capillary pericytes regulate cerebral blood flow in health and disease.
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脑血流量增加，由神经元活动引起，为神经计算提供动力，是BOLD功能成像的基础。血流量是否仅由小动脉平滑肌控制，还是也由毛细血管周细胞控制，这是有争议的。我们证明，神经元的活动和神经递质谷氨酸引起释放的信使扩张毛细血管积极放松周细胞。扩张由前列腺素E2介导，但需要一氧化氮释放来抑制血管收缩的20-HETE合成。在体内，当感觉输入增加血流量时，毛细血管在小动脉之前扩张，估计产生84%的血流量增加。在病理学上，缺血引起周细胞引起毛细血管收缩。我们发现，这是其次是周细胞死亡的僵硬，这可能不可逆地收缩毛细血管和损害血脑屏障。因此，周细胞是脑血流的主要调节者和功能成像信号的启动者。防止周细胞收缩和死亡可能会减少中风后损害神经元的长期血流量减少。
Brain blood flow increases, evoked by neuronal activity, power neural computation and are the basis of BOLD functional imaging. It is controversial whether blood flow is controlled solely by arteriole smooth muscle, or also by capillary pericytes. We demonstrate that neuronal activity and the neurotransmitter glutamate evoke the release of messengers that dilate capillaries by actively relaxing pericytes. Dilation is mediated by prostaglandin E2, but requires nitric oxide release to suppress vasoconstricting 20-HETE synthesis. In vivo, when sensory input increases blood flow, capillaries dilate before arterioles and are estimated to produce 84% of the blood flow increase. In pathology, ischaemia evokes capillary constriction by pericytes. We show that this is followed by pericyte death in rigor, which may irreversibly constrict capillaries and damage the blood-brain barrier. Thus, pericytes are major regulators of cerebral blood flow and initiators of functional imaging signals. Prevention of pericyte constriction and death may reduce the long-lasting blood flow decrease which damages neurons after stroke.