An analysis of modern concepts of the mechanism of the antiradiation effect of alpha1-adrenergic agonists, which are of great interest in clinical practice of radiochemotherapy in cancer patients, has been carried out. The first explanation of their mechanism of action is based on the role of circulatory hypoxia in radiosensitive tissues due to the vasoconstrictor effect of alpha1-adrenergic agonists. During further study of the real decrease in oxygen tension in tissue under circulatory hypoxia, it was found that it is insufficient to fully provide the observed increase in the body’s radioresistance under their influence. The second important fact is that in the course of a decrease in the baseline oxygen consumption per unit of body weight when passing from small to large animals, the antiradiation effect of circulatory and hypoxic hypoxia decreases due to the great adaptive abilities in maintaining oxygen homeostasis of the cell under these conditions. This point is directly related to humans. To explain the high radiation protection in large animals under the influence of alpha1-adrenergic agonists, a hypothesis on the development of acute tissue hypoxia due to the intensification of oxygen consumption under alpha1-adrenergic receptor stimulation has been proposed. The third thesis is that alpha1-adrenergic agonists can stabilize mitochondrial homeostasis under exposure to radiation, thereby reducing the probability of radiation apoptosis of cells and maintaining optimal tissue functioning. All three noted components of the mechanism of the antiradiation effect of alpha1-adrenergic agonists can interact with each other, leading to high protection. The role of each component can change and dominate for each specific scenario of their practical application.

对 α1-肾上腺素能激动剂的抗辐射作用机制的现代概念进行了分析，这在癌症患者放化疗的临床实践中具有重要意义。其作用机制的第一个解释是基于循环缺氧在放射敏感组织中的作用，这是由于 α1-肾上腺素能激动剂的血管收缩作用。在进一步研究循环缺氧条件下组织中氧张力的真正降低时，发现在它们的影响下，不足以完全提供观察到的身体辐射抗性的增加。第二个重要的事实是，在从小型动物到大型动物时，每单位体重的基线耗氧量下降的过程中，由于在这些条件下维持细胞氧稳态的强大适应能力，循环和缺氧缺氧的抗辐射作用降低。这一点与人类直接相关。为了解释在 α1-肾上腺素能受体激动剂影响下大型动物的高辐射防护，提出了一个假设，即由于在 α1-肾上腺素能受体刺激下耗氧量增加而导致急性组织缺氧的发展。第三个论点是α1-肾上腺素能激动剂可以在暴露于辐射下稳定线粒体稳态，从而降低细胞辐射凋亡的可能性并保持最佳组织功能。α1-肾上腺素能激动剂抗辐射作用机制的所有三个提到的组成部分都可以相互作用，导致高保护。每个组件的角色可以改变和支配其实际应用的每个特定场景。