Raybould H E, Roberts M E, Dockray G J
Am J Physiol. 1987 Aug;253(2 Pt 1):G165-70. doi: 10.1152/ajpgi.1987.253.2.G165.
The actions of intravenous sulfated cholecystokinin octapeptide (CCK-8) on intraluminal pressure in the body of the stomach were studied in urethan-anesthetized rats. There was a dose-related decrease in pressure in response to CCK-8 over the range 0.3-33 pmol. Bilateral cervical vagotomy alone reduced the response to CCK-8 and together with splanchnic section abolished it. Hexamethonium also reduced the response. Vagotomy did not change the response to CCK-8 in hexamethonium-treated rats, but celiac ganglionectomy abolished it. Guanethidine and phentolamine, but not propranolol, significantly decreased the response to CCK-8; subsequent vagotomy abolished the response. Similarly, depletion of tissue catecholamines by pretreatment with 6-OH dopamine, reserpine, or celiac ganglionectomy together with vagal section abolished the effect of CCK-8. It concluded that CCK-8 decreases mean intragastric pressure in the rat by pathways involving both vagal and splanchnic nerves. The splanchnic pathway involves an alpha-adrenergic mechanism but is hexamethonium resistant. The vagal pathway is hexamethonium sensitive and nonadrenergic. Similar pathways may mediate the effect of CCK on gastric emptying.
在氨基甲酸乙酯麻醉的大鼠中,研究了静脉注射硫酸化胆囊收缩素八肽(CCK-8)对胃体腔内压力的作用。在0.3 - 33 pmol范围内,CCK-8引起的压力呈剂量依赖性降低。单独双侧颈迷走神经切断术可降低对CCK-8的反应,与内脏神经切断术联合应用则可消除该反应。六甲铵也可降低反应。在六甲铵处理的大鼠中,迷走神经切断术并未改变对CCK-8的反应,但腹腔神经节切除术可消除该反应。胍乙啶和酚妥拉明可显著降低对CCK-8的反应,而普萘洛尔则无此作用;随后进行迷走神经切断术可消除该反应。同样,用6-羟基多巴胺、利血平预处理或腹腔神经节切除术联合迷走神经切断术耗尽组织儿茶酚胺后,CCK-8的作用消失。得出结论:CCK-8通过涉及迷走神经和内脏神经的途径降低大鼠胃内平均压力。内脏神经途径涉及α-肾上腺素能机制,但对六甲铵有抗性。迷走神经途径对六甲铵敏感且无肾上腺素能作用。类似的途径可能介导CCK对胃排空的作用。