Kawakubo Keishi, Akiba Yasutada, Adelson David, Guth Paul H, Engel Eli, Taché Yvette, Kaunitz Jonathan D
Digestive Diseases Division, CURE: Digestive Diseases Research Center, Department of Medicine, University of California, Los Angeles, CA 90073, USA.
Peptides. 2005 Sep;26(9):1580-9. doi: 10.1016/j.peptides.2005.02.023. Epub 2005 Mar 25.
RX 77368 (RX) increases gastric mucosal blood flow by a vagal cholinergic mechanism. The relative roles of mucosal and connective tissue mast cells (MMC and CTMC) were investigated in RX-injected rats. Blood flow and mast cell degranulation were measured after intracisternal RX. RX significantly increased gastric mucosal blood flow, and sequentially degranulated CTMC and MMC. Ketotifen or doxantrazole inhibited the hyperemic response. Ondansetron, RS-039604-90, or famotidine, but not ketanserin or pyrilamine, reduced hyperemia. Mast cells mediate RX-induced gastric hyperemia via 5-HT3, 5-HT4, and H2 receptors; initial increase depends upon CTMC whereas MMC contributes to the later response.
RX 77368（RX）通过迷走胆碱能机制增加胃黏膜血流量。在注射RX的大鼠中研究了黏膜和结缔组织肥大细胞（MMC和CTMC）的相对作用。脑池内注射RX后测量血流量和肥大细胞脱颗粒情况。RX显著增加胃黏膜血流量，并依次使CTMC和MMC脱颗粒。酮替芬或多沙唑抑制充血反应。昂丹司琼、RS-039604-90或法莫替丁可减轻充血，但酮色林或吡苄明则无此作用。肥大细胞通过5-HT3、5-HT4和H2受体介导RX诱导的胃充血；最初的增加依赖于CTMC，而MMC则对后期反应有贡献。
