He D, Chen Z, Zhou W
Department of Otolaryngology, 254 Hospital, Tianjin.
Zhongguo Ying Yong Sheng Li Xue Za Zhi. 1997 Aug;13(3):246-8.
The purpose of this paper is to understand the physiologic feature of the ampullar endolymphatic potential (AEP) in the guinea pigs (n = 35). The high input impedence microelectrode amplifier was used. The effects of asphyxia, furosemide and ischemia on the AEP were observed. The AEP was 4.55 +/- 1.35 mV, (n = 35) in normal. The potential decreased to 2.8 +/- 0.8 mV from the original level in two minutes of asphyxia. When the respirator was turned on the AEP started to rise abruptly after a latency. In all instances there was an overshoot above the preasphyxia level. When furosemide was administered i.v. at 100 mg/kg, no effects were seen in the AEP. After obstruction of the ascending aorta to cause ischemia, the AEP continued to decline until it reached a minimum of -19.4 +/- 1.7 mV in 52.5 +/- 9.6 minutes and slowly returned to zero line in about 150 minutes. There was no obovious effect after furosemide injection. The results suggest that AEP may deffer from as the positive potential in cochlea. It is produced in the specialized cells (dark cells) of the ampullar and has special electro-physiologic characteristics.
本文旨在了解豚鼠（n = 35）壶腹内淋巴电位（AEP）的生理特征。使用了高输入阻抗微电极放大器。观察了窒息、呋塞米和缺血对AEP的影响。正常情况下，AEP为4.55±1.35 mV（n = 35）。窒息两分钟时，电位从原始水平降至2.8±0.8 mV。当打开呼吸机时，AEP在延迟后开始突然上升。在所有情况下，均有超过窒息前水平的过冲。静脉注射100 mg/kg呋塞米时，AEP未见变化。升主动脉阻塞导致缺血后，AEP持续下降，直至在52.5±9.6分钟时降至最低-19.4±1.7 mV，并在约150分钟时缓慢恢复至零线。注射呋塞米后无明显影响。结果表明，AEP可能与耳蜗中的正电位不同。它由壶腹的特殊细胞（暗细胞）产生，并具有特殊的电生理特征。
