COLD-RESTRAINT STRESS INCREASES RAT FECAL PELLET OUTPUT AND COLONIC TRANSIT
COLD-RESTRAINT STRESS INCREASES RAT FECAL PELLET OUTPUT AND COLONIC TRANSIT
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DOI：
10.1152/ajpgi.1990.258.3.g329
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发表时间：
1990-03-01
影响因子：
--
通讯作者：
ORMSBEE, HS
中科院分区：
文献类型：
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作者：
BARONE, FC;DEEGAN, JF;ORMSBEE, HS
系统地评估了冷束缚应激(CRS)期间出现的粪便颗粒产量的增加。自由喂养的大鼠在这些条件下表现出较低的胃溃疡发生率，他们被研究。CRS显著增加了粪便颗粒产量和液体含量。然而，CRS期间产生的排泄量与肠道分泌活动增加或冷束缚相关的躯体运动活动无关，在麻醉动物中也不存在。冷应激和束缚应激在增加粪便产量方面是相加的。减少肠道转运的药物(即B-HT920、可乐定、洛莫替利、氯哌丁胺和力达米定)可显著减少排泄量与剂量相关。抗胆碱能抗分泌药物、抗抑郁药物和镇静剂对排泄量或液体含量几乎没有影响。在CRS期间，胃肠转运的变化并不是导致粪便产量增加的原因。在CRS过程中，小肠下部的转运没有改变，但盲肠有向大肠排出更多内容物的趋势。结肠运输受到CRS的显著影响，CRS消除了逆行运输，使大部分结肠内容物排出。六甲溴铵、硝苯地平、洛哌丁胺和B-HT920以剂量相关的方式减少CRS增加的结肠转运。在CRS期间的几项时间反应和药物抑制研究中，粪便颗粒产量和结肠运输都受到了类似的影响。这些数据表明，CRS似乎改变了中枢神经系统对结肠的输出，并以一种促进结肠转运和排空的方式改变了结肠平滑肌的运动。小肠转运不参与这一现象，在CRS期间受到不同的调节。
Increased fecal pellet output that occurs during cold-restraint stress (CRS) was evaluated systematically. Free-feeding rats, which exhibit a reduced occurrence of gastric ulcers under these conditions, were studied. CRS significantly increased fecal pellet production and fluid content. However, the fecal output produced during CRS was not associated with increased gut secretory activity or somatic motor activity associated with cold restraint and did not occur in anesthetized animals. Cold and restraint stress were additive in producing increased fecal output. Significant dose-related decreases in fecal output were produced by drugs that decrease gut transit (i.e., B-HT 920, clonidine, Lomotil, loperamide, and lidamidine). Anticholinergic-antisecretory drugs, antidepressants, and transquilizers had little effect on fecal output or fluid content. Changes in gastrointestinal transit did not contribute to the increased fecal output during CRS. Transit in the lower small intestine was not altered, but the cecum tended to empty more contents into the large intestine during CRS. Colonic transit was dramatically affected by CRS, which eliminated retrograde transit and produced the evacuation of the majority of colonic contents. The increased colonic transit produced by CRS was decreased in a dose-related fashion by hexamethonium, nifedipine, loperamide, and B-HT 920. In several time-response and drug-inhibition studies during CRS, both fecal pellet output and colonic transit were affected similarly. These data indicate that CRS appears to change central nervous system output to the colon and that it alters colonic smooth muscle motility in a manner that facilitates colonic transit and evacuation. Small intestinal transit is not involved in this phenomenon and is regulated differently during CRS.