Barone F C, Deegan J F, Price W J, Fowler P J, Fondacaro J D, Ormsbee H S
Department of Pharmacology, SmithKline Beecham Pharmaceuticals, King of Prussia, Pennsylvania 19406-0939.
Am J Physiol. 1990 Mar;258(3 Pt 1):G329-37. doi: 10.1152/ajpgi.1990.258.3.G329.
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 tranquilizers 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.
对冷束缚应激（CRS）期间粪便颗粒排出量增加的情况进行了系统评估。研究了自由进食的大鼠，这些大鼠在这些条件下胃溃疡的发生率较低。CRS显著增加了粪便颗粒的产生和液体含量。然而，CRS期间产生的粪便排出量与肠道分泌活动增加或与冷束缚相关的躯体运动活动增加无关，且在麻醉动物中未出现。寒冷和束缚应激在增加粪便排出量方面具有叠加作用。减少肠道转运的药物（即B-HT 920、可乐定、洛哌丁胺、氯苯哌酰胺和利达脒）可使粪便排出量显著减少，且呈剂量相关。抗胆碱能-抗分泌药物、抗抑郁药和镇静剂对粪便排出量或液体含量影响很小。胃肠道转运的变化对CRS期间粪便排出量增加没有影响。小肠下段的转运没有改变，但在CRS期间盲肠倾向于向大肠排空更多内容物。CRS对结肠转运有显著影响，消除了逆行转运并导致大部分结肠内容物排出。六甲铵、硝苯地平、洛哌丁胺和B-HT 920以剂量相关的方式降低了CRS引起的结肠转运增加。在CRS期间的几次时间反应和药物抑制研究中，粪便颗粒排出量和结肠转运受到的影响相似。这些数据表明，CRS似乎改变了中枢神经系统对结肠的输出，并且以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，并且在CRS期间受到不同的调节。
