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作 者:沈新明[1] 苏清芬[1] 钱梓文[1] 张镜如[1]
机构地区:[1]上海医科大学生理学教研室
出 处:《中国药理学报》1994年第5期439-442,共4页Acta Pharmacologica Sinica
摘 要:记录细胞内电位发现四氧嘧啶具有激活和毒化胰岛B细胞的双相作用。在无或2.75mmol·L^(-1)葡萄糖时四氧嘧啶使B细胞膜去极化并诱发短暂的能被ATP敏感钾通道开放剂二氮嗪阻断的放电;在葡萄糖5.5或11.0mmol·L^(-1)时作用减轻或不明显。提示四氧嘧啶的激活作用与关闭ATP敏感的钾通道有关,而高葡萄糖能保护B细胞免受四氧嘧啶的损伤。Microelectrode method for recording membrane potentials was used. It was observed that alloxan possessed stimulative and toxic dual effects on the electric activity of pancreatic B cells. A 10-min exposure to alloxan 14 mmol·L-1 in the perfusion medium without glucose caused a significant depolarization of B cells from - 44±13 mV to -36 ±12 mV (n = 7, P<0. 05) and evoked spikes in B cells. But the spikes disappeared at 24 ± 12 min (n = 8). In the presence of glucose 5. 5 mmol·L-1 or 11. 0 mmol·L-1, the dual effects became weaker or not obvious. After 10-min exposure to diazoxide (an ATP sensitive K± channel opener) 0. 8 mmol·L-1 in the perfusion medium with alloxan 14 mmol·L-1 but devoid of glucose, the amplitude of membrane potential went up from -31 ±11 mV to - 48 ± 21 mV and the mean value of spikes dropped from 31 ± 24 spikes ·min-1 to 5 ± 5 spikes · min-1. It was suggested that the stimulative effect of alloxan was due to blocking of ATP sensitive K± channel and a higher concentration of glucose could prevent B cells from alloxan injury.
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