Department of Vascular Surgery, Dedinje Cardiovascular Institute, Faculty of Medicine, University of Belgrade, Belgrade, Serbia.
Laboratory of Radiobiology and Molecular Genetics, Institute Vinca, University of Belgrade, Belgrade, Serbia.
Angiology. 2014 Sep;65(8):723-32. doi: 10.1177/0003319713503487. Epub 2013 Sep 23.
Acute brain ischemia caused by transient ischemic attack initiates a complex sequence of events in the central nervous system and hypothalamic-pituitary-adrenal (HPA) axis which may ultimately culminate in neuronal and cell damage. The brain is highly susceptible to ischemia and in response to stress shows changes in morphology and chemistry that are largely reversible. These responses are known to modify the function of the HPA axis, but their mechanisms are not yet clear. Duration and size of the HPA axis activation are regulated by corticotropin-releasing hormone, vasopressin (AVP), and glucocorticoids, including cortisol. Numerous studies suggest that activation of these hormones following brain ischemia can result in neurohormonal dysfunction that can exacerbate long-term prognosis following stroke. These studies represent evidence that changes in the HPA axis play an important role in brain ischemia.
短暂性脑缺血发作引起的急性脑缺血会在中枢神经系统和下丘脑-垂体-肾上腺（HPA）轴引发一系列复杂的事件，最终可能导致神经元和细胞损伤。大脑对缺血非常敏感，并且在应激反应中会发生形态和化学变化，这些变化在很大程度上是可逆的。已知这些反应会改变 HPA 轴的功能，但它们的机制尚不清楚。HPA 轴的激活持续时间和大小受促肾上腺皮质激素释放激素、血管加压素（AVP）和糖皮质激素（包括皮质醇）的调节。许多研究表明，脑缺血后这些激素的激活会导致神经激素功能障碍，从而使中风后的长期预后恶化。这些研究表明，HPA 轴的变化在脑缺血中起着重要作用。
