先天性卵圆孔未闭（PFO）与脑梗死相关，目前认为其机制为PFO导致的反常栓塞，但该理论尚有不足。我们前期研究首次在PFO患者中发现了除反常栓塞之外的另一新机制——动态脑血流自动调节（dCA）受损，但机制不明。皮层扩散性抑制（CSD）是近来提出的与脑血流变化相关的理论，而PFO患者存在CSD的诱发因素。本研究结合临床研究和动物实验，从CSD入手，通过对其激活通路的研究，明确PFO致dCA受损的机制。①临床研究：借助PFO封堵术研究手术前后dCA的变化规律及手术前后右心房与股动脉血中与CSD相关的指标（肾上腺素、内皮素-1、一氧化氮）的变化。②动物实验：借助实验用小型猪PFO模型分析造模前后CSD的变化，验证CSD在PFO中的诱发通路是否为肾上腺素/内皮素-1/Na+-/K+-ATP及NO/cGMP/PKG通路。本研究将阐明PFO致dCA受损的机制，为PFO与脑梗死的关系提供重要理论基础。

Patent foramen ovale (PFO) is a widely accepted risk factor for cryptogenic stroke. A widely accepted theory is paradoxical embolism. However, other mechanisms may be involved since this theory cannot fully explain this phenomenon. In our previous study, we found obvious impairment of dynamic cerebral autoregulation in patients with PFO. In this study, there are two parts. 1. Clinical part: assess the cortical spreading depression function by analyzing the changes of epinephrine, endothelin-1 and nitric oxide before and after PFO closure. 2. Animal experiments: assess the cortical spreading depression function by monitoring spreading depression wave. Assess the role of epinephrine/endothelin-1/Na+-/K+-ATPase pathway and NO/cGMP/PKG pathway in CSD in PFO animal model to explore the potential mechanisms between PFO and cryptogenic stroke.