Fujimoto K, Gotoh Y, Ogata S, Tsunada S, Ohyama T, Ootani A, Okamoto K, Sakata T
Department of Internal Medicine, Saga Medical School, Japan.
Obes Res. 1995 Dec;3 Suppl 5:795S-799S. doi: 10.1002/j.1550-8528.1995.tb00502.x.
The aim of the present paper was to summarize histamine-mediated repair of rat intestinal mucosa. To evaluate intestinal repair, we examined lipid transport (an index of intestinal mucosal function) after 15 minutes occlusion of the superior mesenteric artery. Rats were pretreated with alpha-fluoromethylhistidine (a suicide inhibitor of histidine decarboxylase, a synthesizing enzyme of histamine), H1-receptor antagonist (chlorpheniramine maleate), H2-antagonist (cimetidine), or H3-antagonist (thioperamide) before ischemia-reperfusion (I/R). Lipid transport to rat mesenteric lymph decreased significantly 24 hours after I/R in all groups tested compared to sham-treated rats. Lipid transport was restored 48 hours after I/R in the vehicle-pretreated control group. Lipid transport was not restored to the control level 48 hours after I/R in rats pretreated with H1-antagonist and a suicide inhibitor of histidine decarboxylase. In contrast, intestinal function was restored to the control level 48 hours after I/R in rats pretreated with H2- and H3-antagonists. These results support our previous findings that newly formed histamine after I/R plays an important role in mucosal recovery through H1-receptors.
本文的目的是总结组胺介导的大鼠肠黏膜修复。为评估肠修复情况，我们在肠系膜上动脉闭塞15分钟后检测了脂质转运（肠黏膜功能指标）。在缺血再灌注（I/R）前，大鼠分别用α-氟甲基组氨酸（组胺合成酶组氨酸脱羧酶的自杀性抑制剂）、H1受体拮抗剂（马来酸氯苯那敏）、H2拮抗剂（西咪替丁）或H3拮抗剂（硫代哌啶）进行预处理。与假手术组大鼠相比，所有受试组在I/R后24小时，大鼠肠系膜淋巴中的脂质转运均显著降低。在载体预处理的对照组中，脂质转运在I/R后48小时恢复。在用H1拮抗剂和组氨酸脱羧酶自杀性抑制剂预处理的大鼠中，脂质转运在I/R后48小时未恢复到对照水平。相反，在用H2和H3拮抗剂预处理的大鼠中，肠功能在I/R后48小时恢复到对照水平。这些结果支持了我们之前的发现，即I/R后新形成的组胺通过H1受体在黏膜恢复中起重要作用。
