Nagasaki M, Yamada K, Ikezawa K, Tamaki H
Biological Research Laboratory, Tanabe Seiyaku Co., Ltd., Saitama, Japan.
Nihon Heikatsukin Gakkai Zasshi. 1989 Feb;25(1):27-30. doi: 10.1540/jsmr1965.25.27.
In this study we investigated the involvement of opioid receptors in the contractile response to trimebutine using with the proximal colon of anesthetized rats. Trimebutine (3 mg/kg i.v.) enhanced spontaneous contractions of the proximal colon in anesthetized rats. The contractile response was partially inhibited by intravenous administration of an opioid antagonist, naloxone at 1 approximately 30 micrograms/kg, but was hardly depressed by intracisternal administration of naloxone (30 micrograms/kg). Morphine (30 micrograms/kg i.v.) evoked colonic contractions which were abolished by intravenous naloxone (30 micrograms/kg). These results suggest that the colonic contractions evoked by trimebutine in anesthetized rats are, in part, mediated by peripheral opioid receptors.
在本研究中，我们使用麻醉大鼠的近端结肠来研究阿片受体在曲美布汀收缩反应中的作用。曲美布汀（3毫克/千克静脉注射）增强了麻醉大鼠近端结肠的自发收缩。静脉注射阿片拮抗剂纳洛酮（1至30微克/千克）可部分抑制收缩反应，但脑池内注射纳洛酮（30微克/千克）几乎不能使其抑制。吗啡（30微克/千克静脉注射）引起结肠收缩，静脉注射纳洛酮（30微克/千克）可消除这种收缩。这些结果表明，麻醉大鼠中曲美布汀引起的结肠收缩部分是由外周阿片受体介导的。
