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观察铃蟾肽（ＢＯＭ） 对豚鼠离体肠系膜下神经节（ＩＭＧ） 细胞基本电生理学特性的影响及其初步的离子作用机制。方法 应用细胞内微电极记录技术，运用压力注射法和灌流法给药。结果 ①ＢＯＭ（１０ －５ ｍｏｌ·Ｌ－１） 压力注射至ＩＭＧ 细胞周围（ ｎ＝１８０） ，８４－０ ％ 的细胞出现去极化反应；８－３ ％ 的细胞出现先超极化后去极化反应；７－７ ％ 的细胞无明显反应。②蛙皮素（１０ －７ ｍｏｌ·Ｌ－ １ ～１０ －６ ｍｏｌ·Ｌ－ １） 灌流ＩＭＧ（ｎ ＝ １０） ，９０ ％ 的细胞出现去极化反应。③ＢＯＭ 去极化反应中膜电阻增大的细胞占５－０ ％ ；膜电阻减小者占６０－０ ％ ；膜电阻不变者占３５－０ ％ 。④低钙／ 高镁溶液使５６－３ ％ 的去极化反应幅度减小，３１－２ ％ 被完全阻抑，而１２－５ ％ 的去极化反应不受影响。⑤ＢＯＭ 去极化反应不为胆碱受体阻断剂（ 阿托品和筒箭毒，１０ －３ ｍｏｌ·Ｌ－１） 所阻断（ ｎ ＝ ５） ，也不为肾上腺素能受体阻断剂（ 酚妥拉明和心得安，１０ －３ｍｏｌ·Ｌ－１） 所阻断（ｎ ＝ ６） 。⑥低钠溶液（ ｎ ＝ ６） 和高钾溶液（ｎ ＝ ６） 灌流皆阻抑ＢＯＭ 去极化反应。⑦控制细胞膜电位（ ｎ ＝ １２） ，见ＢＯＭ 去极化
To observe the effect of bombesin (BOM) on the basic electrophysiological characteristics of guinea pig isolated in vitro mesenteric ganglion (IMG) cells and its primary ion mechanism. Methods Intracellular microelectrode recording technique was used to apply pressure injection and perfusion method. Results ① BOM (10 -5 mol·L-1) was injected into the periphery of IMG cells (n = 180), 84-0% of the cells depolarized; 8-3% of the cells appeared hyperpolarized and then depolarized The reaction; 7-7% of the cells no significant reaction. ② Bone morphogenetic protein (10 -7 mol·L -1 -10 -6 mol·L -1) was used to perfuse IMG (n = 10). 90% of the cells were depolarized. ③ BOM depolarization reaction increased membrane resistance cells accounted for 5-0%; membrane resistance decreased by 60-0%; membrane resistance unchanged accounted for 35-0%. ④ The low-calcium / high-magnesium solution reduced the 56-3% of the depolarization reaction amplitude, while the 31-2% was completely suppressed, while the 12-5% depolarization reaction was unaffected. ⑤ BOM depolarization was not blocked by cholinergic receptor blockers (atropine and mycotoxin, 10 -3 mol·L-1) (n = 5), nor was adrenergic receptor blockers (Phentolamine and propranolol, 10 -3 mol·L-1) (n = 6). (6) Perfusion of low sodium solution (n = 6) and high potassium solution (n = 6) all inhibited BOM depolarization. ⑦ control cell membrane potential (n = 12), see BOM depolarization