Citation

Fujimoto K, Gotoh Y, Ogata S, Tsunada S, Ohyama T, Ootani A, Okamoto K, Sakata T. Obes. Res. 1995; 3 Suppl 5: 795S-799S.

Copyright

(Copyright © 1995, North American Association for the Study of Obesity)

DOI

10.1002/j.1550-8528.1995.tb00502.x

PMID

8653565

Abstract

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.

Language: en

Keywords

Animals; Biological Transport; Chlorpheniramine; Cimetidine; Enzyme Inhibitors; Histamine; Histamine Antagonists; Histamine H1 Antagonists; Histamine H2 Antagonists; Histidine Decarboxylase; Intestinal Mucosa; Ischemia; Lipid Metabolism; Lymph; Male; Methylhistidines; Piperidines; Rats; Rats, Sprague-Dawley; Reperfusion