Siesjö B K
University of Lund, Laboratory for Experimental Brain Research, Sweden.
Prog Brain Res. 1993;96:1-9. doi: 10.1016/s0079-6123(08)63255-0.
The last 20-30 years of research has brought detailed information on the pathophysiology and the neurochemistry of anoxic/ischemic brain damage. On the basis of this information, important mediators of such damage have been identified, notably loss of calcium homeostasis, excessive acidosis and enhanced production of free radicals. At present, the tools of basic neuroscience are being employed to unravel the cellular and molecular mechanisms involved. The results suggest that the second and third messengers expressed as a result of a calcium transient may be instrumental in triggering cell damage. These encompass excessive activation of protein kinases and phosphatases, and expression of new genes. The new data emerging in this field herald the advent of new concepts which can explain the causes of ischemic/anoxic brain damage in molecular terms.
过去二三十年的研究已带来了关于缺氧/缺血性脑损伤的病理生理学和神经化学的详细信息。基于这些信息，已确定了此类损伤的重要介质，尤其是钙稳态的丧失、过度酸中毒和自由基产生增加。目前，基础神经科学工具正被用于揭示其中涉及的细胞和分子机制。结果表明，由钙瞬变导致表达的第二和第三信使可能在引发细胞损伤中起作用。这些包括蛋白激酶和磷酸酶的过度激活以及新基因的表达。该领域出现的新数据预示着能够从分子层面解释缺血/缺氧性脑损伤原因的新概念的出现。
