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内源性胆囊收缩素抑制自由活动清醒大鼠的结肠收缩。

Endogenous CCK inhibits colonic contractions in unrestrained conscious rats.

作者信息

Hayashi K, Kishimoto S, Kannbe M

机构信息

Department of Geriatric Medicine, Institute of Health Sciences, Hiroshima University School of Medicine, Japan.

出版信息

Regul Pept. 1997 Oct 31;72(2-3):131-7. doi: 10.1016/s0167-0115(97)01051-3.

Abstract

As cholecystokinin octapeptide (CCK-OP) and feeding have been reported to relax the circular muscle contractions of the proximal colon in unrestrained conscious rats under fasting conditions, the, action of cholecystokinin, released after duodenal infusion of a low residual diet of clinimeal, was studied on the motor activity of the proximal colon in unrestrained conscious rats. We used an implantable telemetry system with a miniature strain gauge force transducer introduced into the rat proximal colon. By using a specific radioimmunoassay system for CCK, plasma levels of CCK before and after duodenal infusion of clinimeal (0.5, 1.0, 2.0 ml) were determined at 0, 5, 10, 20, 30, 60 min in the portal blood. The clinimeal infusion caused a significant increase in CCK levels of the portal plasma during 5 and 30 min. This increase was in a dose-dependent manner. In accordance with this increase in plasma CCK, the motor activity of the proximal circular muscle was suppressed significantly. A bolus injection of the CCK A receptor antagonist, loxiglumide, CR 1505 (0.1, 0.5 and 1.0 mg/kg ip), prior to clinimeal blocked the inhibitory action of CCK on the motor activity in a concentration-dependent manner. These data suggest that endogenous CCK released by a residual diet is involved in the mechanism of inhibition of motor activity in the proximal colon.

摘要

据报道,在禁食条件下,胆囊收缩素八肽(CCK-OP)和进食可使自由活动的清醒大鼠近端结肠的环形肌收缩松弛,因此,本研究观察了十二指肠灌注低残留量临床营养膳食后释放的胆囊收缩素对自由活动的清醒大鼠近端结肠运动活性的作用。我们使用了一种可植入式遥测系统,该系统带有一个微型应变片力传感器,将其植入大鼠近端结肠。通过使用一种针对CCK的特异性放射免疫分析系统,在门静脉血中于0、5、10、20、30、60分钟时测定十二指肠灌注临床营养膳食(0.5、1.0、2.0毫升)前后的CCK血浆水平。临床营养膳食灌注在5至30分钟期间导致门静脉血浆中CCK水平显著升高。这种升高呈剂量依赖性。与血浆CCK的这种升高相一致,近端环形肌的运动活性被显著抑制。在灌注临床营养膳食之前,静脉注射CCK A受体拮抗剂洛莫司汀(CR 1505,0.1、0.5和1.0毫克/千克)可浓度依赖性地阻断CCK对运动活性的抑制作用。这些数据表明,残留膳食释放的内源性CCK参与了近端结肠运动活性抑制机制。

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