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目的和方法：观察犬脑干缺血不同时点递质性氨基酸含量的变化及其与神经元损伤的关系，以探讨递质性氨基酸在脑干缺血损伤中的可能作用。结果：犬脑干缺血３０ｍｉｎ，兴奋性氨基酸（ＥＡＡｓ）递质含量升高不明显，神经元呈轻度缺血损伤；缺血３ｈ后，ＥＡＡｓ含量显著升高，并随着缺血时间的延长不断增加，神经元亦从中度发展至重度缺血损伤。抑制性氨基酸（ＩＡＡｓ）递质在缺血３ｈ后开始有显著升高；至缺血１２ｈ，两者不再增高。即使在缺血后期，ＩＡＡｓ有明显增高，神经元损伤仍无减轻迹象。结论：ＥＡＡｓ参与了脑干缺血损伤病理过程；脑干缺血后期增高的ＩＡＡｓ对缺血损伤的神经保护作用表现不明显
Aims and Methods: To observe the changes of the levels of neurotransmitters and neuronal damage in different time points of canine brainstem ischemia to explore the possible role of neurotransmitter amino acids in ischemic brain stem injury. Results: After ischemia for 30 min, the content of neurotransmitter EAA did not increase obviously and the neurons showed mild ischemic injury. After 3 h of ischemia, the content of EAAs increased significantly, and with the time of ischemia Increasing the extension of neurons from moderate to severe ischemic injury. Inhibitory amino acids (IAAs) neurotransmitters began to significantly increase 3h after ischemia; to ischemia 12h, both no longer increased. Even in the late phase of ischemia, IAAs were significantly increased, and neuronal damage still showed no sign of reduction. CONCLUSION: EAAs are involved in the pathological process of ischemic injury of brain stem. The neuroprotective effect of IAAs increased in the late stage of brain stem ischemia on ischemic injury is insignificant