Barkhatov D Iu, Dzhibladze D N, Barkhatova V P
Zh Nevrol Psikhiatr Im S S Korsakova. 2006;106(4):10-4.
A study of the functional state of cerebral hemodynamics using transcranial dopplerography and blood excitotoxic amino acids, playing an important role in the pathogenesis of ischemic brain damage, has been carried out in 43 patients with atherosclerotic lesions of the carotid arteries. Neurological deficit that developed as a result of ischemic stroke was related to the changes of cerebral hemodynamics (a decrease of hemodynamic reserve and blood flow velocity in the middle cerebral artery) and an increase of the level of blood amino acids involved in excitotoxic mechanisms of the nerve tissue lesions in brain ischemia. These biochemical disturbances in the non-acute period of ischemic stroke may be explained by the state of chronic excitotoxicity that developed because of blood circulation insufficiency in the brain and a decrease of cerebrovascular reserve. The authors admit that genetically determined features of cerebral metabolism of excitotoxic amino acids, concomitant with their higher release to the extracellular space, along with hemodynamical disturbances, may be risk factors of ischemic brain lesion when cerebral blood flow decreased as a result of stenosis or occlusion of the carotid arteries. This should be taken into account for elaboration of complex methods of neuroprotection in atherosclerosis of the great brain arteries.
对43例颈动脉粥样硬化病变患者进行了一项研究,该研究采用经颅多普勒超声检查和血液兴奋性毒性氨基酸来评估脑血流动力学的功能状态,血液兴奋性毒性氨基酸在缺血性脑损伤的发病机制中起重要作用。缺血性中风导致的神经功能缺损与脑血流动力学的变化(血流动力学储备降低和大脑中动脉血流速度减慢)以及参与脑缺血神经组织损伤兴奋性毒性机制的血液氨基酸水平升高有关。缺血性中风非急性期的这些生化紊乱可能是由于脑循环不足和脑血管储备降低导致的慢性兴奋性毒性状态所致。作者承认,当由于颈动脉狭窄或闭塞导致脑血流量减少时,兴奋性毒性氨基酸脑代谢的遗传决定特征,以及它们向细胞外空间的更高释放,连同血流动力学紊乱,可能是缺血性脑损伤的危险因素。在制定大脑动脉粥样硬化的综合神经保护方法时应考虑到这一点。