Barber P A, Auer R N, Buchan A M, Sutherland G R
Department of Clinical Neurosciences, Seaman Family Magnetic Resonance Research Centre, University of Calgary, AB, Canada.
Can J Physiol Pharmacol. 2001 Mar;79(3):283-96.
Transient or permanent focal brain injury following acute thromboembolic occlusion develops from a complex cascade of pathophysiological events. The processes of excitotoxicity, peri-infarct depolarisation, inflammation, and apoptosis within the ischemic penumbra are proposed. While the translation of therapeutic agents from the animal models to human clinical trials have been disappointing, there remains an atmosphere of optimism as a result of the development of new diagnostic and therapeutic approaches, which include physiological, as opposed to pharmacological, intervention. This article provides an insight into the understanding of cerebral ischemia, together with current and future treatment strategies.
急性血栓栓塞性闭塞后发生的短暂性或永久性局灶性脑损伤是由一系列复杂的病理生理事件级联反应所致。有人提出了缺血半暗带内的兴奋性毒性、梗死灶周围去极化、炎症和凋亡等过程。尽管从动物模型到人类临床试验的治疗药物转化一直不尽人意,但由于新诊断和治疗方法的发展,包括生理性而非药理学干预,仍存在乐观的氛围。本文深入探讨了对脑缺血的理解以及当前和未来的治疗策略。