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本实验在海马脑片采用微电极记录技术，观察了缺氧损伤电位（ＨＩＰ）的电生理特性，并研究了其产生机制。实验结果表明：①ＨＩＰ是突触在缺氧过程中功能暂时恢复的反应；②随着缺氧程度的加重，ＨＩＰ出现时间前移，持续时间缩短；③ＨＩＰ的出现表明突触功能的丧失发生在突触膜损伤之前，其消失代表突触传递不可逆性损伤的发生，即突触膜损伤的开始；④大剂量腺苷不能阻止ＨＩＰ的产生，表明ＨＩＰ的出现不是由于腺苷浓度的降低。
In this study, microelectrode recording technique was used in hippocampal slices to observe the electrophysiological characteristics of hypoxic injury potential (HIP) and to study its mechanism. The experimental results showed that: (1) HIP is a transient response to synaptic function during hypoxia; (2) HIP appears to move forward with a shortened duration as hypoxia progresses; (3) the presence of HIP indicates that the loss of synaptic function occurs during the process of hypoxia Before the injury of the traumatic membrane, its disappearance represents the occurrence of irreversible damage of synaptic transmission, that is, the onset of synaptic membrane injury. (4) The high dose of adenosine can not prevent the production of HIP, indicating that the occurrence of HIP is not due to the decrease of adenosine concentration.