Abstract：
Whether cerebral sympathetic-mediated vasomotor control can be modulated by local brain activity remains unknown. This study tested the hypothesis that the application or removal of a cognitive task during a cold pressor test (CPT) would attenuate and restore decreases in cerebrovascular conductance (CVC), respectively. Middle cerebral artery blood velocity (transcranial Doppler) and mean arterial pressure (finger photoplethysmography) were examined in healthy adults (n = 16; 8 females and 8 males) who completed a control CPT, followed by a CPT coupled with a cognitive task administered either 1) 30 s after the onset of the CPT and for the duration of the CPT or 2) at the onset of the CPT and terminated 30 s before the end of the CPT (condition order was counterbalanced). The major finding was that the CPT decreased the index of CVC, and such decreases were abolished when a cognitive task was completed concurrently and restored when the cognitive task was removed. As a secondary experiment, vasomotor interactions between sympathetic transduction pathways (α1-adrenergic and Y1-peptidergic) and compounds implicated in cerebral blood flow control [adenosine, and adenosine triphosphate (ATP)] were explored in isolated porcine cerebral arteries (wire myography). The data reveal α1-receptor agonism potentiated vasorelaxation modestly in response to adenosine, and preexposure to ATP attenuated contractile responses to α1-agonism. Overall, the data suggest a cognitive task attenuates decreases in CVC during sympathoexcitation, possibly related to an interaction between purinergic and α1-adrenergic signaling pathways.NEW & NOTEWORTHY The present study demonstrates that the cerebrovascular conductance index decreases during sympathoexcitation and this response can be positively and negatively modulated by the application or withdrawal of a nonexercise cognitive task. Furthermore, isolated vessel experiments reveal that cerebral α1-adrenergic agonism potentiates adenosine-mediated vasorelaxation and ATP attenuates α1-adrenergic-mediated vasocontraction.
摘要：
脑交感神经介导的血管舒缩控制是否可以通过局部脑活动来调节仍然未知。这项研究测试了以下假设：在冷加压测试（CPT）期间应用或消除认知任务会减弱和恢复脑血管电导（CVC）的下降。分别。在完成对照CPT的健康成年人（n=16;8F和8M）中检查了大脑中动脉血流速度（经颅多普勒）和平均动脉压（手指光体积描记术）。随后是CPT，再加上认知任务，分别在CPT开始后30s和CPT持续时间或B）在CPT开始时进行，并在CPT结束前30s终止（抵消了条件顺序）。主要发现是CPT降低了CVC指数，当同时完成认知任务时，这种减少被消除，当移除认知任务时，这种减少被恢复。作为次要实验,交感神经传导途径（α1肾上腺素能和Y1肽能）与脑血流控制中涉及的化合物（腺苷，和三磷酸腺苷（ATP））在分离的猪脑动脉（线肌电图）中进行了研究。数据显示，α1受体激动作用对腺苷的反应适度增强了血管舒张，和预暴露于ATP减弱了对α1激动的收缩反应。总的来说,数据表明认知任务减弱了交感神经兴奋期间CVC的降低，可能与嘌呤能和α1-肾上腺素能信号通路之间的相互作用有关。
