Experimental Studies on Developmental Mechanism of Histamine Induced Ulcers and Ulcer Inhibitory Effects of Histamine Receptor Antagonists

アクセス数 : 816
ダウンロード数 : 99

今月のアクセス数 : 0
今月のダウンロード数 : 0
File
HiroshimaJMedSci_32_311.pdf 1.09 MB 種類 : fulltext
Title ( eng )
Experimental Studies on Developmental Mechanism of Histamine Induced Ulcers and Ulcer Inhibitory Effects of Histamine Receptor Antagonists
Title ( jpn )
ヒスタミン潰瘍発生機序ならびにヒスタミン受容体拮抗剤の潰瘍抑制効果
Creator
Kodama Motomu
Ogawa Yoshiteru
Ito Nobuaki
Takeuchi Hitoshi
Seikoh Rokuro
Tanaka Tsuneo
Harada Mitsuo
Kodama Osamu
Ezaki Haruo
Source Title
Hiroshima Journal of Medical Sciences
Volume 32
Issue 3
Start Page 311
End Page 318
Journal Identifire
[PISSN] 0018-2052
[EISSN] 2433-7668
[NCID] AA00664312
Abstract
Study was made of the developmental mechanism of histamine induced ulcers and inhibitory effects of receptor antagonists from the view point of gastric acidity and microvasculature of the gastric mucosa, and the following results were obtained.

1. In histamine induced ulcers, hypersecretion of gastric acid caused by histamine is not the primary developmental mechanism of the lesion. The main cause is considered to be disturbance of microcirculation in the gastric mucosa attributable to the effects of histamine on the microvasculature of the mucosa.

2. Of the histamine receptor antagonists, diphenhydramine, an Hi-antagonist, was unable to inhibit hypersecretion of gastric acid and disturbance of microcirculation of the gastric mucosa caused by histamine, and thus could not suppress the development of histamine induced ulcers, but cimetidine, an H2-antagonist, inhibited not only hypersecretion of gastric acid, but also prevent disturbance of microcirculation in the mucosa, and consequently suppressed histamine induced ulcers.
Keywords
Histamine induced ulcer
Histamine receptor antagonists
NDC
Medical sciences [ 490 ]
Language
eng
Resource Type departmental bulletin paper
Publisher
Hiroshima University School of Medicine
Date of Issued 1983-09
Publish Type Version of Record
Access Rights open access
Source Identifier
[ISSN] 0018-2052
[NCID] AA00664312
[PMID] 6643109