Leukotriene D4 excitation of rabbit distal colon arises in the region of the muscularis mucosae.
Leukotriene D4 excitation of rabbit distal colon arises in the region of the muscularis mucosae.
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白三烯 D4 对兔远端结肠的兴奋发生在粘膜肌层区域。
DOI：
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发表时间：
1990
影响因子：
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通讯作者：
R. Burakoff
中科院分区：
文献类型：
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作者：
W. H. Percy;S. Y. Lee;M. Burton;T. Tolentino;R. Burakoff
我们之前已经在体内证明，动脉内注射白三烯 D4 (LTD4) 会导致兔远端结肠的肌电和机械活动增加。本研究的目的是利用体内和体外技术来尝试阐明这种效应的机制。在体内，用阿托品（0.1 mg/kg iv）或六甲铵（5 mg/kg iv）或LTD4受体拮抗剂SK&F 102922（0.8微克/kg ia）预处理消除了兔远端结肠对LTD4的兴奋反应。在体外，纵向肌层和环状肌层均未对LTD4（10（-10）至10（-7）M）产生收缩反应。在相同浓度范围内，LTD4引起粘膜肌层收缩，这种收缩被SK&F 102922（10（-9）至10（-7）M）或吲哚美辛（10（-6）M）减弱，但不受阿托品（10（-6）M）、吡拉明（10（-6）M）或河鲀毒素（10（-6）M）影响。米）。纵向肌、环肌和粘膜肌层的全层节段未收缩至LTD4。这些数据暗示体内LTD4诱导的兔子远端结肠的兴奋是由于粘膜肌层区域的LTD4受体兴奋而产生的，并且这最终导致乙酰胆碱释放到固有肌层上。有人提出，导致后一种效应的一种可能机制是由于前列腺素诱导的对冲击粘膜下神经丛的神经释放的去甲肾上腺素的抑制而导致内在神经的兴奋性增加。
We previously have demonstrated in vivo that intra-arterial administration of leukotriene D4 (LTD4) causes increased myoelectric and mechanical activity in the rabbit distal colon. The aim of this study was to use both in vivo and in vitro techniques to try to elucidate the mechanism underlying this effect. In vivo the excitatory response of the rabbit distal colon to LTD4 was abolished by pretreatment with atropine (0.1 mg/kg iv) or hexamethonium (5 mg/kg iv) or the LTD4 receptor antagonist SK&F 102922 (0.8 micrograms/kg ia). In vitro neither the longitudinal nor the circular muscle layer responded to LTD4 (10(-10) to 10(-7) M) with a contractile response. Over the same concentration range, LTD4 caused contractions of the muscularis mucosae that were attenuated by either SK&F 102922 (10(-9) to 10(-7) M) or indomethacin (10(-6) M) but were unaffected by atropine (10(-6) M), pyrilamine (10(-6) M), or tetrodotoxin (10(-6) M). Full thickness segments of longitudinal muscle, circular muscle, and muscularis mucosae did not contract to LTD4. These data imply that LTD4-induced excitation of the rabbit distal colon in vivo arises as a result of the excitation of LTD4 receptors in the region of the muscularis mucosae and that this leads ultimately to the release of acetylcholine onto the muscularis propria. It is proposed that one possible mechanism leading to the latter effect is an increased excitability of intrinsic nerves resulting from a prostaglandin-induced depression of norepinephrine release from nerves impinging on the submucosal plexus.