DOSE-RELATED EFFECTS OF SYNTHETIC HUMAN BETA-ENDORPHIN AND NALOXONE ON FED GASTROINTESTINAL MOTILITY
DOSE-RELATED EFFECTS OF SYNTHETIC HUMAN BETA-ENDORPHIN AND NALOXONE ON FED GASTROINTESTINAL MOTILITY
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DOI：
10.1152/ajpgi.1986.251.1.g147
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发表时间：
1986-07-01
影响因子：
--
通讯作者：
LI, CH
中科院分区：
文献类型：
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作者：
CAMILLERI, M;MALAGELADA, JR;LI, CH
在人类中，血浆β-内啡肽水平在施加急性应激刺激（眩晕、冷痛和经皮电刺激）期间升高，所述急性应激刺激诱发肠运动紊乱。然而，有可能循环的β-虽然内啡肽参与调节这些对肠道运动的中枢作用，但它的作用不能仅仅根据血浆水平的变化来确定。因此，我们设计了本研究以研究静脉内合成的人β-内啡肽和纳洛酮对进食的健康个体的胃肠道压力活动的影响;以及阿片激动剂和拮抗剂的相互作用。注入β-内啡肽增加幽门阶段性压力活动（P < 0.001），并诱导肠节律性活动爆发（P < 0.05），中断正常进食运动。这些效应与剂量相关，幽门剂量-反应曲线基本呈线性。在近端肠中的作用是用β-内啡肽250 ng. cntdot. kg-1. min-1或更大。在胃窦中，阶段性压力活动总体上降低（P < 0.02），这主要是对高剂量的β-受体阻滞剂的作用。内啡肽输注（2，500 ng. kg-1. min ~（-1）。纳洛酮本身对进食后上消化道运动无显著影响。然而，纳洛酮显著抑制较低剂量的β-幽门的内啡肽此外，纳洛酮显着降低了β-的可能性内啡肽，引发肠道的节律性活动。这些数据表明，β-内啡肽可能在生理水平上刺激进食幽门收缩中起体液作用。此外，β-内啡肽对人的进食胃窦和肠运动表现出强烈的药理作用。
In humans, plasma .beta.-endorphin levels rise during application of acute stressful stimuli (vertigo, cold pain, and transcutaneous electrical stimulation) that induce gut motor disturbances. Whereas it is possible that circulating .beta.-endorphin participates in the mediation of these central effects on gut motility, its role cannot be established solely on the basis of changes in plasma levels. Therefore, we designed the present study to investigate the dose-related effects of intravenous synthetic human .beta.-endorphin and naloxone on gastrointestinal pressure activity in fed healthy individuals; and the interactions of the opiate agonist and antagonist. Infusion of .beta.-endorphin increased pyloric phasic pressure activity (P < 0.001) and induced intestinal bursts of rhythmic activity (P < 0.05) which interrupted normal fed motility. These effects were dose related, with the pyloric dose-response profile being essentially linear. The effects in the proximal intestine were obtained with doses of .beta.-endorphin at 250 ng .cntdot. kg-1 .cntdot. min-1 or greater. In the antrum, there was an overall reduction in phasic pressure activity (P < 0.02), which was predominantly in an effect on the high dose of .beta.-endorphin infused (2,500 ng .cntdot. kg-1 .cntdot. min-1). Naloxone by itself had no significant effect on fed upper gut motility. However, naloxone significantly inhibited the effects of the lower doses of .beta.-endorphin on the pylorus. In addition, naloxone significantly reduced the probability of .beta.-endorphin, triggering intestinal bursts of rhythmic activity. These data suggest that .beta.-endorphin may play a humoral role in the stimulation of fed pyloric contraction at physiological levels. Furthermore, .beta.-endorphin exhibits strong pharmacological actions on fed antral and intestinal motility in humans.