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氯胺酮在体外可保护海马神经元免受缺氧损伤。

Ketamine protects hippocampal neurons from anoxia in vitro.

作者信息

Rothman S M, Thurston J H, Hauhart R E, Clark G D, Solomon J S

出版信息

Neuroscience. 1987 Jun;21(3):673-8. doi: 10.1016/0306-4522(87)90028-5.

Abstract

Ketamine, a dissociative, general anesthetic, blocks the excitation produced by activating one class of excitatory amino acid receptors, the N-methyl-D-aspartate receptor in the rat. We have found that ketamine can protect hippocampal neurons in culture and slice from anoxia. When added to cultures immediately prior to anoxic exposure, ketamine prevented the neuronal destruction seen after a day of anoxia. Neurons appeared undamaged and had normal resting and action potentials. Adenosine triphosphate levels in ketamine-protected anoxic cultures were approximately two-thirds of normal controls. Ketamine also prevented the irreversible loss of the population spike seen in hippocampal slices after prolonged perfusion with anoxic buffer. These results suggest that ketamine may have therapeutic potential in preventing anoxic damage from stroke in man.

摘要

氯胺酮是一种分离性全身麻醉剂,可阻断大鼠体内一类兴奋性氨基酸受体(N-甲基-D-天冬氨酸受体)激活所产生的兴奋作用。我们发现,氯胺酮可保护培养和切片中的海马神经元免受缺氧损伤。在缺氧暴露前立即添加到培养物中时,氯胺酮可防止缺氧一天后出现的神经元破坏。神经元看起来未受损,且静息电位和动作电位正常。氯胺酮保护的缺氧培养物中的三磷酸腺苷水平约为正常对照的三分之二。氯胺酮还可防止在用缺氧缓冲液长时间灌注后海马切片中出现的群体峰电位不可逆丧失。这些结果表明,氯胺酮在预防人类中风缺氧损伤方面可能具有治疗潜力。

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